Dupage APA-86 - History

Dupage APA-86 - History

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Dupage I

A county in Illinois.

(APA_41 dp. 7,846: 1. 491'8": b. 69'6": dr. 26'6": n,
17 k.; cpl. 640; a. 2 5"; cl. Bagfield)

The first DuPage (AP-86) was launched 19 December 1942 as Sea Hound by Ingalls Shipbuilding Co., Pascagoula, Miss., under a Maritime Commission contract; sponsored by Mrs. Leigh R. Sanford. reclassified APA-41, 1 February 1943; placed in ferry commission 28 February 1943, Commander C. Allen in command; decommisioned 17 March 1943 for conversion by ToddErie Basin Dry Docks, Brooklyn, N.Y., and commissioned 1 September 1943, Captain G. M. Wauchope, USNR, in command.

DuPage reached San Diego from Norfolk 2 November 1943 to serve as flagship for a transport division during training. She sailed from San Diego 13 January 1944 carrying Marina for the assault landings on Kwajalein, where she remained from 31 January to 6 February. DuPage sailed by way of Funafuti, Ellice Islands, to Guadalcanal, arriving 18 February.

Based at Guadalcanal DuPage served in the redeployment of troops in the Solomons and carried troops for the assault landings at Emirau Island on 11 April 1944 and the support landings at Cape Gloucester, New Britain, from 28 April to 1 May. On 3 June she got underway for the invasion of Guam, landing her troops from 21 to 26 July. After evacuating casualties to Eniwetok, and exercising off Espiritu Santo, DuPage returned to Guadalcanal 27 August to replenish, overhaul her landing craft, and train for the invasion of the Palau Islands.

DuPage sortied from Guadalcanal 8 September 1944 and landed her troops in the assault of' Peleliu a week later. For 12 days she remained in the area providing logistics support for landing craft and small patrol vessels. Three of her own landing craft were lost and one man killed during the bitter fighting. Arriving at Hollandia, New Guinea, 3o September, DuPage prepared for the invasion of the Philippines. She carried Army troops for the initial landings at Leyte on 20 October and sailed at once to bring reinforcements from Hollandia for support landings on 14 November. |

After rehearsal landings in New Guinea, Dupage sailed from Aitape 28 December 1944 for the invasion of Lingayen Gulf, landing her troops on the beaches near San Fabian 9 January 1945 and embarking casualties from the beach and other ships. On the evening of the next day while DuPage was preparing to leave the area. enemy aircraft attacked. Despite the heavy antiaircraft fire, a kamikaze crashed to port damaging her severely as well as starting fires which stubbornly recurred and were fought all through the night. She lost 35 killed and 136 wounded, 5 men who were blown over the side were picked up by an escorting destroyer several hours later. Despite her injuries DuPage continued to furfill her duty as guide ship and arrived safely at Leyte 3 days later to transfer her casualties and undergo emergency repairs.

After landing troops at Zambales, Luzon on 29 January 1945, DuPage left San Pedro Bay 11 February and embarking Marines at Manus and Pearl Harbor en route, arrived at San Francisco 10 March for overhaul and battle damage repairs. She sailed from Alameda 14 May to embark troops at Seattle, Wash, for Pearl Harbor. She continued to Eniwetok for amphibious exercises, then transported troops and cargo from Ulithi to Okinawa' arriving 5 July. Three days later she sailed with combat-tested Marines for Guam, then continued to Eniwetok and San Francisco where she arrived 28 July. After minor alterations she was designated as flagship for Transport Division 63 and sailed 12 August with Army Air Force personnel whom she disembarked at San Pedro Bay, Leyte, 5 September.

DuPage sailed from Lingayen Gulf, 1 October 1945 with troops for the occupation of Japan, landing her passengers at Nagoya on 26 October. Three days later she was assigned to "Magic Carpet" duty and made two voyages between Guam and the west coast to return veterans until 5 January 1946 when she arrived at Portland, Oreg. Two weeks later she got underway for the east coast, arriving at New York 7 February. DuPage was decommissioned 28 March 1946 and transferred to the War Shipping Administration for disposal 27 June 1946.

DuPage received six battle stars for World War II service.

The second DuPage (APB-51) was self-propelled barracks ship which operated in a noncommissioned status providing Special Services with advanced bases,Pacific area, during 1951-59.

DuPage County, Illinois

DuPage County ( / ˌ d uː ˈ p eɪ dʒ / ) is a county in the U.S. state of Illinois, and one of the collar counties of the Chicago metropolitan area. As of the 2010 census, the population was 916,924, [2] making it Illinois' second-most populous county. Its county seat is Wheaton. [3]

Known for its vast Tallgrass prairies, DuPage County has become mostly developed and suburbanized, although some pockets of farmland remain in the county's western and northern parts. Located in the Rust Belt, the area is one of few in the region whose economy quickly became dependant on the headquarters of several large corporations due to its close proximity to Chicago. As steel mills closed in the 1970's and 80's, several acres that were formally industrialized areas were converted into business parks to meet the growing tax base. The county has a mixed socioeconomic profile and residents of Hinsdale, Naperville and Oak Brook include some of the wealthiest people in the Midwest. On the whole, the county enjoys above average median household income levels and low overall poverty levels when compared to the national average. [4] In 2018, Niche ranked two DuPage municipalities (Clarendon Hills #3 and Naperville #16) amongst the top 20 best places to live in America. [5]



In the United States, dextromethamphetamine hydrochloride, under the trade name Desoxyn, has been approved by the FDA for treating ADHD and obesity in both adults and children [22] [23] however, the FDA also indicates that the limited therapeutic usefulness of methamphetamine should be weighed against the inherent risks associated with its use. [22] Methamphetamine is sometimes prescribed off label for narcolepsy and idiopathic hypersomnia. [24] [25] In the United States, methamphetamine's levorotary form is available in some over-the-counter (OTC) nasal decongestant products. [note 3]

As methamphetamine is associated with a high potential for misuse, the drug is regulated under the Controlled Substances Act and is listed under Schedule II in the United States. [22] Methamphetamine hydrochloride dispensed in the United States is required to include a boxed warning regarding its potential for recreational misuse and addiction liability. [22]


Methamphetamine is often used recreationally for its effects as a potent euphoriant and stimulant as well as aphrodisiac qualities. [26]

According to a National Geographic TV documentary on methamphetamine, an entire subculture known as party and play is based around sexual activity and methamphetamine use. [26] Participants in this subculture, which consists almost entirely of homosexual male methamphetamine users, will typically meet up through internet dating sites and have sex. [26] Due to its strong stimulant and aphrodisiac effects and inhibitory effect on ejaculation, with repeated use, these sexual encounters will sometimes occur continuously for several days on end. [26] The crash following the use of methamphetamine in this manner is very often severe, with marked hypersomnia (excessive daytime sleepiness). [26] The party and play subculture is prevalent in major US cities such as San Francisco and New York City. [26] [27]

Methamphetamine is contraindicated in individuals with a history of substance use disorder, heart disease, or severe agitation or anxiety, or in individuals currently experiencing arteriosclerosis, glaucoma, hyperthyroidism, or severe hypertension. [22] The FDA states that individuals who have experienced hypersensitivity reactions to other stimulants in the past or are currently taking monoamine oxidase inhibitors should not take methamphetamine. [22] The FDA also advises individuals with bipolar disorder, depression, elevated blood pressure, liver or kidney problems, mania, psychosis, Raynaud's phenomenon, seizures, thyroid problems, tics, or Tourette syndrome to monitor their symptoms while taking methamphetamine. [22] Due to the potential for stunted growth, the FDA advises monitoring the height and weight of growing children and adolescents during treatment. [22]


The physical effects of methamphetamine can include loss of appetite, hyperactivity, dilated pupils, flushed skin, excessive sweating, increased movement, dry mouth and teeth grinding (leading to "meth mouth"), headache, irregular heartbeat (usually as accelerated heartbeat or slowed heartbeat), rapid breathing, high blood pressure, low blood pressure, high body temperature, diarrhea, constipation, blurred vision, dizziness, twitching, numbness, tremors, dry skin, acne, and pale appearance. [22] [29] Long-term meth users may have sores on their skin [30] [31] [32] these may be caused by scratching due to itchiness [31] or the belief that insects are crawling under their skin, [30] and the damage is compounded by poor diet and hygiene. [32] Numerous deaths related to methamphetamine overdoses have also been reported as well. [33] [34]

Meth mouth

Methamphetamine users and addicts may lose their teeth abnormally quickly, regardless of the route of administration, from a condition informally known as meth mouth. [35] The condition is generally most severe in users who inject the drug, rather than swallow, smoke, or inhale it. [35] According to the American Dental Association, meth mouth "is probably caused by a combination of drug-induced psychological and physiological changes resulting in xerostomia (dry mouth), extended periods of poor oral hygiene, frequent consumption of high-calorie, carbonated beverages and bruxism (teeth grinding and clenching)". [35] [36] As dry mouth is also a common side effect of other stimulants, which are not known to contribute severe tooth decay, many researchers suggest that methamphetamine associated tooth decay is more due to users' other choices. They suggest the side effect has been exaggerated and stylized to create a stereotype of current users as a deterrence for new ones. [23]

Sexually transmitted infection

Methamphetamine use was found to be related to higher frequencies of unprotected sexual intercourse in both HIV-positive and unknown casual partners, an association more pronounced in HIV-positive participants. [37] These findings suggest that methamphetamine use and engagement in unprotected anal intercourse are co-occurring risk behaviors, behaviors that potentially heighten the risk of HIV transmission among gay and bisexual men. [37] Methamphetamine use allows users of both sexes to engage in prolonged sexual activity, which may cause genital sores and abrasions as well as priapism in men. [22] [38] Methamphetamine may also cause sores and abrasions in the mouth via bruxism, increasing the risk of sexually transmitted infection. [22] [38]

Besides the sexual transmission of HIV, it may also be transmitted between users who share a common needle. [39] The level of needle sharing among methamphetamine users is similar to that among other drug injection users. [39]


Doses of 200 mg or more of methamphetamine are considered fatal. [40]


The psychological effects of methamphetamine can include euphoria, dysphoria, changes in libido, alertness, apprehension and concentration, decreased sense of fatigue, insomnia or wakefulness, self-confidence, sociability, irritability, restlessness, grandiosity and repetitive and obsessive behaviors. [22] [29] [41] Peculiar to methamphetamine and related stimulants is "punding", persistent non-goal-directed repetitive activity. [42] Methamphetamine use also has a high association with anxiety, depression, amphetamine psychosis, suicide, and violent behaviors. [43]

Neurotoxic and neuroimmunological

Methamphetamine is directly neurotoxic to dopaminergic neurons in both lab animals and humans. [20] [21] Excitotoxicity, oxidative stress, metabolic compromise, UPS dysfunction, protein nitration, endoplasmic reticulum stress, p53 expression and other processes contributed to this neurotoxicity. [47] [48] [49] In line with its dopaminergic neurotoxicity, methamphetamine use is associated with a higher risk of Parkinson's disease. [50] In addition to its dopaminergic neurotoxicity, a review of evidence in humans indicated that high-dose methamphetamine use can also be neurotoxic to serotonergic neurons. [21] It has been demonstrated that a high core temperature is correlated with an increase in the neurotoxic effects of methamphetamine. [51] Withdrawal of methamphetamine in dependent persons may lead to post-acute withdrawal which persists months beyond the typical withdrawal period. [49]

Magnetic resonance imaging studies on human methamphetamine users have also found evidence of neurodegeneration, or adverse neuroplastic changes in brain structure and function. [21] In particular, methamphetamine appears to cause hyperintensity and hypertrophy of white matter, marked shrinkage of hippocampi, and reduced gray matter in the cingulate cortex, limbic cortex, and paralimbic cortex in recreational methamphetamine users. [21] Moreover, evidence suggests that adverse changes in the level of biomarkers of metabolic integrity and synthesis occur in recreational users, such as a reduction in N-acetylaspartate and creatine levels and elevated levels of choline and myoinositol. [21]

Methamphetamine has been shown to activate TAAR1 in human astrocytes and generate cAMP as a result. [50] Activation of astrocyte-localized TAAR1 appears to function as a mechanism by which methamphetamine attenuates membrane-bound EAAT2 (SLC1A2) levels and function in these cells. [50]

Methamphetamine binds to and activates both sigma receptor subtypes, σ1 and σ2, with micromolar affinity. [46] [52] Sigma receptor activation may promote methamphetamine-induced neurotoxicity by facilitating hyperthermia, increasing dopamine synthesis and release, influencing microglial activation, and modulating apoptotic signaling cascades and the formation of reactive oxygen species. [46] [52]


  • addiction – a biopsychosocial disorder characterized by persistent use of drugs (including alcohol) despite substantial harm and adverse consequences
  • addictive drug – psychoactive substances that with repeated use are associated with significantly higher rates of substance use disorders, due in large part to the drug's effect on brain reward systems
  • dependence – an adaptive state associated with a withdrawal syndrome upon cessation of repeated exposure to a stimulus (e.g., drug intake)
  • drug sensitization or reverse tolerance – the escalating effect of a drug resulting from repeated administration at a given dose
  • drug withdrawal – symptoms that occur upon cessation of repeated drug use
  • physical dependence – dependence that involves persistent physical–somatic withdrawal symptoms (e.g., fatigue and delirium tremens)
  • psychological dependence – dependence that involves emotional–motivational withdrawal symptoms (e.g., dysphoria and anhedonia)
  • reinforcing stimuli – stimuli that increase the probability of repeating behaviors paired with them
  • rewarding stimuli – stimuli that the brain interprets as intrinsically positive and desirable or as something to approach
  • sensitization – an amplified response to a stimulus resulting from repeated exposure to it
  • substance use disorder – a condition in which the use of substances leads to clinically and functionally significant impairment or distress
  • tolerance – the diminishing effect of a drug resulting from repeated administration at a given dose

Current models of addiction from chronic drug use involve alterations in gene expression in certain parts of the brain, particularly the nucleus accumbens. [64] [65] The most important transcription factors [note 4] that produce these alterations are ΔFosB, cAMP response element binding protein (CREB), and nuclear factor kappa B (NFκB). [65] ΔFosB plays a crucial role in the development of drug addictions, since its overexpression in D1-type medium spiny neurons in the nucleus accumbens is necessary and sufficient [note 5] for most of the behavioral and neural adaptations that arise from addiction. [54] [65] [67] Once ΔFosB is sufficiently overexpressed, it induces an addictive state that becomes increasingly more severe with further increases in ΔFosB expression. [54] [67] It has been implicated in addictions to alcohol, cannabinoids, cocaine, methylphenidate, nicotine, opioids, phencyclidine, propofol, and substituted amphetamines, among others. [65] [67] [68] [69] [70]

ΔJunD, a transcription factor, and G9a, a histone methyltransferase enzyme, both directly oppose the induction of ΔFosB in the nucleus accumbens (i.e., they oppose increases in its expression). [54] [65] [71] Sufficiently overexpressing ΔJunD in the nucleus accumbens with viral vectors can completely block many of the neural and behavioral alterations seen in chronic drug use (i.e., the alterations mediated by ΔFosB). [65] ΔFosB also plays an important role in regulating behavioral responses to natural rewards, such as palatable food, sex, and exercise. [65] [68] [72] Since both natural rewards and addictive drugs induce expression of ΔFosB (i.e., they cause the brain to produce more of it), chronic acquisition of these rewards can result in a similar pathological state of addiction. [65] [68] ΔFosB is the most significant factor involved in both amphetamine addiction and amphetamine-induced sex addictions, which are compulsive sexual behaviors that result from excessive sexual activity and amphetamine use. [note 6] [68] [73] These sex addictions (i.e., drug-induced compulsive sexual behaviors) are associated with a dopamine dysregulation syndrome which occurs in some patients taking dopaminergic drugs, such as amphetamine or methamphetamine. [68] [72] [73]

Epigenetic factors

Methamphetamine addiction is persistent for many individuals, with 61% of individuals treated for addiction relapsing within one year. [74] About half of those with methamphetamine addiction continue with use over a ten-year period, while the other half reduce use starting at about one to four years after initial use. [75]

The frequent persistence of addiction suggests that long-lasting changes in gene expression may occur in particular regions of the brain, and may contribute importantly to the addiction phenotype. Recently a crucial role has been found for epigenetic mechanisms in driving lasting changes in gene expression in the brain. [76]

A review in 2015 [77] summarized a number of studies involving chronic methamphetamine use in rodents. Epigenetic alterations were observed in the brain reward pathways, including areas like ventral tegmental area, nucleus accumbens, and dorsal striatum, the hippocampus, and the prefrontal cortex. Chronic methamphetamine use caused gene-specific histone acetylations, deacetylations and methylations. Gene-specific DNA methylations in particular regions of the brain were also observed. The various epigenetic alterations caused downregulations or upregulations of specific genes important in addiction. For instance, chronic methamphetamine use caused methylation of the lysine in position 4 of histone 3 located at the promoters of the c-fos and the C-C chemokine receptor 2 (ccr2) genes, activating those genes in the nucleus accumbens (NAc). [77] c-fos is well known to be important in addiction. [78] The ccr2 gene is also important in addiction, since mutational inactivation of this gene impairs addiction. [77]

In methamphetamine addicted rats, epigenetic regulation through reduced acetylation of histones, in brain striatal neurons, caused reduced transcription of glutamate receptors. [79] Glutamate receptors play an important role in regulating the reinforcing effects of misused illicit drugs. [80]

Treatment and management

A 2018 systematic review and network meta-analysis of 50 trials involving 12 different psychosocial interventions for amphetamine, methamphetamine, or cocaine addiction found that combination therapy with both contingency management and community reinforcement approach had the highest efficacy (i.e., abstinence rate) and acceptability (i.e., lowest dropout rate). [81] Other treatment modalities examined in the analysis included monotherapy with contingency management or community reinforcement approach, cognitive behavioral therapy, 12-step programs, non-contingent reward-based therapies, psychodynamic therapy, and other combination therapies involving these. [81]

As of December 2019 [update] , there is no effective pharmacotherapy for methamphetamine addiction. [82] [83] [84] A systematic review and meta-analysis from 2019 assessed the efficacy of 17 different pharmacotherapies used in RCTs for amphetamine and methamphetamine addiction [83] it found only low-strength evidence that methylphenidate might reduce amphetamine or methamphetamine self-administration. [83] There was low- to moderate-strength evidence of no benefit for most of the other medications used in RCTs, which included antidepressants (bupropion, mirtazapine, sertraline), antipsychotics (aripiprazole), anticonvulsants (topiramate, baclofen, gabapentin), naltrexone, varenicline, citicoline, ondansetron, prometa, riluzole, atomoxetine, dextroamphetamine, and modafinil. [83]

Dependence and withdrawal

Tolerance is expected to develop with regular methamphetamine use and, when used recreationally, this tolerance develops rapidly. [85] [86] In dependent users, withdrawal symptoms are positively correlated with the level of drug tolerance. [87] Depression from methamphetamine withdrawal lasts longer and is more severe than that of cocaine withdrawal. [88]

According to the current Cochrane review on drug dependence and withdrawal in recreational users of methamphetamine, "when chronic heavy users abruptly discontinue [methamphetamine] use, many report a time-limited withdrawal syndrome that occurs within 24 hours of their last dose". [87] Withdrawal symptoms in chronic, high-dose users are frequent, occurring in up to 87.6% of cases, and persist for three to four weeks with a marked "crash" phase occurring during the first week. [87] Methamphetamine withdrawal symptoms can include anxiety, drug craving, dysphoric mood, fatigue, increased appetite, increased movement or decreased movement, lack of motivation, sleeplessness or sleepiness, and vivid or lucid dreams. [87]

Methamphetamine that is present in a mother's bloodstream can pass through the placenta to a fetus and be secreted into breast milk. [88] Infants born to methamphetamine-abusing mothers may experience a neonatal withdrawal syndrome, with symptoms involving of abnormal sleep patterns, poor feeding, tremors, and hypertonia. [88] This withdrawal syndrome is relatively mild and only requires medical intervention in approximately 4% of cases. [88]

Summary of addiction-related plasticity
Form of neuroplasticity
or behavioral plasticity
Type of reinforcer Sources
Opiates Psychostimulants High fat or sugar food Sexual intercourse Physical exercise
ΔFosB expression in
nucleus accumbens D1-type MSNs
Behavioral plasticity
Escalation of intake Yes Yes Yes [68]
Yes Not applicable Yes Yes Attenuated Attenuated [68]
conditioned place preference
Reinstatement of drug-seeking behavior [68]
Neurochemical plasticity
CREB phosphorylation
in the nucleus accumbens
Sensitized dopamine response
in the nucleus accumbens
No Yes No Yes [68]
Altered striatal dopamine signaling ↓DRD2, ↑DRD3 ↑DRD1, ↓DRD2, ↑DRD3 ↑DRD1, ↓DRD2, ↑DRD3 ↑DRD2 ↑DRD2 [68]
Altered striatal opioid signaling No change or
↑μ-opioid receptors
↑μ-opioid receptors
↑κ-opioid receptors
↑μ-opioid receptors ↑μ-opioid receptors No change No change [68]
Changes in striatal opioid peptides ↑dynorphin
No change: enkephalin
↑dynorphin ↓enkephalin ↑dynorphin ↑dynorphin [68]
Mesocorticolimbic synaptic plasticity
Number of dendrites in the nucleus accumbens [68]
Dendritic spine density in
the nucleus accumbens


Unlike other drugs, babies with prenatal exposure to methamphetamines don't show immediate signs of withdrawal. Instead, cognitive and behavioral problems start emerging when the children reach school age. [89]

A prospective cohort study of 330 children showed that at the age of 3, children with methamphetamine exposure showed increased emotional reactivity, as well as more signs of anxiety and depression and at the age of 5, children showed higher rates of externalizing and attention deficit/hyperactivity disorders. [90]

A methamphetamine overdose may result in a wide range of symptoms. [4] [22] A moderate overdose of methamphetamine may induce symptoms such as: abnormal heart rhythm, confusion, difficult and/or painful urination, high or low blood pressure, high body temperature, over-active and/or over-responsive reflexes, muscle aches, severe agitation, rapid breathing, tremor, urinary hesitancy, and an inability to pass urine. [4] [29] An extremely large overdose may produce symptoms such as adrenergic storm, methamphetamine psychosis, substantially reduced or no urine output, cardiogenic shock, bleeding in the brain, circulatory collapse, hyperpyrexia (i.e., dangerously high body temperature), pulmonary hypertension, kidney failure, rapid muscle breakdown, serotonin syndrome, and a form of stereotypy ("tweaking"). [sources 1] A methamphetamine overdose will likely also result in mild brain damage due to dopaminergic and serotonergic neurotoxicity. [94] [21] Death from methamphetamine poisoning is typically preceded by convulsions and coma. [22]


Use of methamphetamine can result in a stimulant psychosis which may present with a variety of symptoms (e.g., paranoia, hallucinations, delirium, and delusions). [4] [95] A Cochrane Collaboration review on treatment for amphetamine, dextroamphetamine, and methamphetamine use-induced psychosis states that about 5–15% of users fail to recover completely. [95] [96] The same review asserts that, based upon at least one trial, antipsychotic medications effectively resolve the symptoms of acute amphetamine psychosis. [95] Amphetamine psychosis may also develop occasionally as a treatment-emergent side effect. [97]

Emergency treatment

Acute methamphetamine intoxication is largely managed by treating the symptoms and treatments may initially include administration of activated charcoal and sedation. [4] There is not enough evidence on hemodialysis or peritoneal dialysis in cases of methamphetamine intoxication to determine their usefulness. [22] Forced acid diuresis (e.g., with vitamin C) will increase methamphetamine excretion but is not recommended as it may increase the risk of aggravating acidosis, or cause seizures or rhabdomyolysis. [4] Hypertension presents a risk for intracranial hemorrhage (i.e., bleeding in the brain) and, if severe, is typically treated with intravenous phentolamine or nitroprusside. [4] Blood pressure often drops gradually following sufficient sedation with a benzodiazepine and providing a calming environment. [4]

Antipsychotics such as haloperidol are useful in treating agitation and psychosis from methamphetamine overdose. [98] [99] Beta blockers with lipophilic properties and CNS penetration such as metoprolol and labetalol may be useful for treating CNS and cardiovascular toxicity. [100] The mixed alpha- and beta-blocker labetalol is especially useful for treatment of concomitant tachycardia and hypertension induced by methamphetamine. [98] The phenomenon of "unopposed alpha stimulation" has not been reported with the use of beta-blockers for treatment of methamphetamine toxicity. [98]

Methamphetamine is metabolized by the liver enzyme CYP2D6, so CYP2D6 inhibitors will prolong the elimination half-life of methamphetamine. [101] Methamphetamine also interacts with monoamine oxidase inhibitors (MAOIs), since both MAOIs and methamphetamine increase plasma catecholamines therefore, concurrent use of both is dangerous. [22] Methamphetamine may decrease the effects of sedatives and depressants and increase the effects of antidepressants and other stimulants as well. [22] Methamphetamine may counteract the effects of antihypertensives and antipsychotics due to its effects on the cardiovascular system and cognition respectively. [22] The pH of gastrointestinal content and urine affects the absorption and excretion of methamphetamine. [22] Specifically, acidic substances will reduce the absorption of methamphetamine and increase urinary excretion, while alkaline substances do the opposite. [22] Due to the effect pH has on absorption, proton pump inhibitors, which reduce gastric acid, are known to interact with methamphetamine. [22]


Methamphetamine has been identified as a potent full agonist of trace amine-associated receptor 1 (TAAR1), a G protein-coupled receptor (GPCR) that regulates brain catecholamine systems. [102] [103] Activation of TAAR1 increases cyclic adenosine monophosphate (cAMP) production and either completely inhibits or reverses the transport direction of the dopamine transporter (DAT), norepinephrine transporter (NET), and serotonin transporter (SERT). [102] [104] When methamphetamine binds to TAAR1, it triggers transporter phosphorylation via protein kinase A (PKA) and protein kinase C (PKC) signaling, ultimately resulting in the internalization or reverse function of monoamine transporters. [102] [105] Methamphetamine is also known to increase intracellular calcium, an effect which is associated with DAT phosphorylation through a Ca2+/calmodulin-dependent protein kinase (CAMK)-dependent signaling pathway, in turn producing dopamine efflux. [106] [107] [108] TAAR1 has been shown to reduce the firing rate of neurons through direct activation of G protein-coupled inwardly-rectifying potassium channels. [109] [110] [111] TAAR1 activation by methamphetamine in astrocytes appears to negatively modulate the membrane expression and function of EAAT2, a type of glutamate transporter. [50]

In addition to its effect on the plasma membrane monoamine transporters, methamphetamine inhibits synaptic vesicle function by inhibiting VMAT2, which prevents monoamine uptake into the vesicles and promotes their release. [112] This results in the outflow of monoamines from synaptic vesicles into the cytosol (intracellular fluid) of the presynaptic neuron, and their subsequent release into the synaptic cleft by the phosphorylated transporters. [113] Other transporters that methamphetamine is known to inhibit are SLC22A3 and SLC22A5. [112] SLC22A3 is an extraneuronal monoamine transporter that is present in astrocytes, and SLC22A5 is a high-affinity carnitine transporter. [103] [114]

Methamphetamine is also an agonist of the alpha-2 adrenergic receptors and sigma receptors with a greater affinity for σ1 than σ2, and inhibits monoamine oxidase A (MAO-A) and monoamine oxidase B (MAO-B). [46] [103] [52] Sigma receptor activation by methamphetamine may facilitate its central nervous system stimulant effects and promote neurotoxicity within the brain. [46] [52] Dextromethamphetamine is a stronger psychostimulant, but levomethamphetamine has stronger peripheral effects, a longer half-life, and longer perceived effects among addicts. [115] [116] [117] At high doses, both enantiomers of methamphetamine can induce similar stereotypy and methamphetamine psychosis, [116] but levomethamphetamine has shorter psychodynamic effects. [117]


Following oral administration, methamphetamine is well-absorbed into the bloodstream, with peak plasma methamphetamine concentrations achieved in approximately 3.13–6.3 hours post ingestion. [118] Methamphetamine is also well absorbed following inhalation and following intranasal administration. [4] Due to the high lipophilicity of methamphetamine, it can readily move through the blood–brain barrier faster than other stimulants, where it is more resistant to degradation by monoamine oxidase. [4] [118] The amphetamine metabolite peaks at 10–24 hours. [4] Methamphetamine is excreted by the kidneys, with the rate of excretion into the urine heavily influenced by urinary pH. [22] [118] When taken orally, 30–54% of the dose is excreted in urine as methamphetamine and 10–23% as amphetamine. [118] Following IV doses, about 45% is excreted as methamphetamine and 7% as amphetamine. [118] The half-life of methamphetamine is variable with a range of 5–30 hours. [4]

CYP2D6, dopamine β-hydroxylase, flavin-containing monooxygenase 3, butyrate-CoA ligase, and glycine N-acyltransferase are the enzymes known to metabolize methamphetamine or its metabolites in humans. [sources 2] The primary metabolites are amphetamine and 4-hydroxymethamphetamine [118] other minor metabolites include: 4-hydroxyamphetamine , 4-hydroxynorephedrine , 4-hydroxyphenylacetone , benzoic acid, hippuric acid, norephedrine, and phenylacetone, the metabolites of amphetamine. [6] [118] [119] Among these metabolites, the active sympathomimetics are amphetamine, 4‑hydroxyamphetamine , [125] 4‑hydroxynorephedrine , [126] 4-hydroxymethamphetamine , [118] and norephedrine. [127] Methamphetamine is a CYP2D6 inhibitor. [101]

The main metabolic pathways involve aromatic para-hydroxylation, aliphatic alpha- and beta-hydroxylation, N-oxidation, N-dealkylation, and deamination. [6] [118] [128] The known metabolic pathways include:

Detection in biological fluids

Methamphetamine and amphetamine are often measured in urine or blood as part of a drug test for sports, employment, poisoning diagnostics, and forensics. [131] [132] [133] [134] Chiral techniques may be employed to help distinguish the source of the drug to determine whether it was obtained illicitly or legally via prescription or prodrug. [135] Chiral separation is needed to assess the possible contribution of levomethamphetamine, which is an active ingredients in some OTC nasal decongestants, [note 3] toward a positive test result. [135] [136] [137] Dietary zinc supplements can mask the presence of methamphetamine and other drugs in urine. [138]

Methamphetamine is a chiral compound with two enantiomers, dextromethamphetamine and levomethamphetamine. At room temperature, the free base of methamphetamine is a clear and colorless liquid with an odor characteristic of geranium leaves. [9] It is soluble in diethyl ether and ethanol as well as miscible with chloroform. [9] In contrast, the methamphetamine hydrochloride salt is odorless with a bitter taste. [9] It has a melting point between 170 and 175 °C (338 and 347 °F) and, at room temperature, occurs as white crystals or a white crystalline powder. [9] The hydrochloride salt is also freely soluble in ethanol and water. [9]


A 2011 study into the destruction of methamphetamine using bleach showed that effectiveness is correlated with exposure time and concentration. [139] A year-long study (also from 2011) showed that methamphetamine in soils is a persistent pollutant. [140] In a 2013 study of bioreactors in wastewater, methamphetamine was found to be largely degraded within 30 days under exposure to light. [141]


Racemic methamphetamine may be prepared starting from phenylacetone by either the Leuckart [142] or reductive amination methods. [143] In the Leuckart reaction, one equivalent of phenylacetone is reacted with two equivalents of N-methylformamide to produce the formyl amide of methamphetamine plus carbon dioxide and methylamine as side products. [143] In this reaction, an iminium cation is formed as an intermediate which is reduced by the second equivalent of N-methylformamide . [143] The intermediate formyl amide is then hydrolyzed under acidic aqueous conditions to yield methamphetamine as the final product. [143] Alternatively, phenylacetone can be reacted with methylamine under reducing conditions to yield methamphetamine. [143]

Amphetamine, discovered before methamphetamine, was first synthesized in 1887 in Germany by Romanian chemist Lazăr Edeleanu who named it phenylisopropylamine. [146] [147] Shortly after, methamphetamine was synthesized from ephedrine in 1893 by Japanese chemist Nagai Nagayoshi. [148] Three decades later, in 1919, methamphetamine hydrochloride was synthesized by pharmacologist Akira Ogata via reduction of ephedrine using red phosphorus and iodine. [149]

Since 1938, methamphetamine was marketed on a large scale in Germany as a nonprescription drug under the brand name Pervitin, produced by the Berlin-based Temmler pharmaceutical company. [150] [151] It was used by all branches of the combined Wehrmacht armed forces of the Third Reich, for its stimulant effects and to induce extended wakefulness. [152] [153] Pervitin became colloquially known among the German troops as "Stuka-Tablets" (Stuka-Tabletten) and "Herman-Göring-Pills" (Hermann-Göring-Pillen). Side effects were so serious that the army sharply cut back its usage in 1940. [154] By 1941, usage was restricted to a doctor's prescription, and the military tightly controlled its distribution. Soldiers would only receive a couple tablets at a time, and were discouraged from using them in combat. Historian Lukasz Kamienski says "A soldier going to battle on Pervitin usually found himself unable to perform effectively for the next day or two. Suffering from a drug hangover and looking more like a zombie than a great warrior, he had to recover from the side effects." Some soldiers turned very violent, committing war crimes against civilians others attacked their own officers. [154]

At the end of the war, it was used as part of a new drug: D-IX.

Obetrol, patented by Obetrol Pharmaceuticals in the 1950s and indicated for treatment of obesity, was one of the first brands of pharmaceutical methamphetamine products. [155] Due to the psychological and stimulant effects of methamphetamine, Obetrol became a popular diet pill in America in the 1950s and 1960s. [155] Eventually, as the addictive properties of the drug became known, governments began to strictly regulate the production and distribution of methamphetamine. [147] For example, during the early 1970s in the United States, methamphetamine became a schedule II controlled substance under the Controlled Substances Act. [156] Currently, methamphetamine is sold under the trade name Desoxyn, trademarked by the Danish pharmaceutical company Lundbeck. [157] As of January 2013, the Desoxyn trademark had been sold to Italian pharmaceutical company Recordati. [158]

The Golden Triangle (Southeast Asia), specifically Shan State, Myanmar, is the world's leading producer of methamphetamine as production has shifted to Yaba and crystalline methamphetamine, including for export to the United States and across East and Southeast Asia and the Pacific. [159]

Concerning the accelerating synthetic drug production in the region, the Cantonese Chinese syndicate Sam Gor, also known as The Company, is understood to be the main international crime syndicate responsible for this shift. [160] It is made up of members of five different triads. Sam Gor is primarily involved in drug trafficking, earning at least $8 billion per year. [161] Sam Gor is alleged to control 40% of the Asia-Pacific methamphetamine market, while also trafficking heroin and ketamine. The organization is active in a variety of countries, including Myanmar, Thailand, New Zealand, Australia, Japan, China, and Taiwan. Sam Gor previously produced meth in Southern China and is now believed to manufacture mainly in the Golden Triangle, specifically Shan State, Myanmar, responsible for much of the massive surge of crystal meth in recent years. [162] The group is understood to be headed by Tse Chi Lop, a gangster born in Guangzhou, China who also holds a Canadian passport.

The production, distribution, sale, and possession of methamphetamine is restricted or illegal in many jurisdictions. [163] [164] Methamphetamine has been placed in schedule II of the United Nations Convention on Psychotropic Substances treaty. [164]

It has been suggested, based on animal research, that calcitriol, the active metabolite of vitamin D, can provide significant protection against the DA- and 5-HT-depleting effects of neurotoxic doses of methamphetamine. [165]


Ivermectin is used to treat human diseases caused by roundworms and ectoparasites.

Worm infections

For river blindness (onchocerciasis) and lymphatic filariasis, ivermectin is typically given as part of mass drug administration campaigns that distribute the drug to all members of a community affected by the disease. [20] For river blindness, a single oral dose of ivermectin (150 micrograms per kilogram of body weight) clears the body of larval Onchocerca volvulus worms for several months, preventing transmission and disease progression. [20] Adult worms survive in the skin and eventually recover to produce larval worms again. To keep the worms at bay, ivermectin is given at least once per year for the 10–15-year lifespan of the adult worms. [21] For lymphatic filariasis, oral ivermectin (200 micrograms per kilogram body weight) is part of a combination treatment given annually: ivermectin, diethylcarbamazine citrate and albendazole in places without onchocerciasis ivermectin and albendazole in places with onchocerciasis. [22] [note 1]

The World Health Organization considers ivermectin the "drug of choice" for strongyloidiasis. [24] Most cases are treated with two daily doses of oral ivermectin (200 μg per kg body weight), while severe infections are treated with five to seven days of ivermectin. [20] Ivermectin is also the primary treatment for Mansonella ozzardi and cutaneous larva migrans. [25] [26] The U.S. Centers for Disease Control recommends ivermectin, albendazole, or mebendazole as treatments for ascariasis. [27] [note 2] Ivermectin is sometimes added to albendazole or mebendazole for whipworm treatment, and is considered a second-line treatment for gnathostomiasis. [26] [31]

Mites and insects

Ivermectin is also used to treat infection with parasitic arthropods. Scabies – infestation with the mite Sarcoptes scabiei – is most commonly treated with topical permethrin or oral ivermectin. For most scabies cases, ivermectin is used in a two dose regimen: a first dose kills the active mites, but not their eggs. Over the next week, the eggs hatch, and a second dose kills the newly hatched mites. [32] [33] For severe "crusted scabies", the Centers for Disease Control recommends up to seven doses of ivermectin over the course of a month, along with a topical antiparasitic. [33] Both head lice and pubic lice can be treated with oral ivermectin, a 0.5% ivermection lotion applied directly to the affected area, or various other insecticides. [34] [35] Ivermectin is also used to treat rosacea and blepharitis, both of which can be caused or exacerbated by Demodex folliculorum mites. [36] [37]

Ivermectin is contraindicated in children under the age of five or those who weigh less than 15 kilograms (33 pounds), [38] and individuals with liver or kidney disease. [39] Ivermectin is secreted in very low concentration in breast milk. [40] It remains unclear if ivermectin is safe during pregnancy. [41]

Serious adverse events following ivermectin treatment are more common in people with very high burdens of larval Loa loa worms in their blood. [42] Those who have over 30,000 microfilaria per milliliter of blood risk inflammation and capillary blockage due to the rapid death of the microfilaria following ivermectin treatment. [42]

The main concern is neurotoxicity, which in most mammalian species may manifest as central nervous system depression, and consequent ataxia, as might be expected from potentiation of inhibitory GABA-ergic synapses.

Since drugs that inhibit the enzyme CYP3A4 often also inhibit P-glycoprotein transport, the risk of increased absorption past the blood-brain barrier exists when ivermectin is administered along with other CYP3A4 inhibitors. These drugs include statins, HIV protease inhibitors, many calcium channel blockers, lidocaine, the benzodiazepines, and glucocorticoids such as dexamethasone. [43]

During the course of a typical treatment, ivermectin can cause minor aminotransferase elevations and, rarely, mild clinically apparent liver disease. [44]

For dogs, the insecticide spinosad may have the effect of increasing the toxicity of ivermectin. [45]

Mechanism of action

Ivermectin and its related drugs act by interfering with nerve and muscle function of helminths and insects. [46] The drug binds to glutamate-gated chloride channels that are common to invertebrate nerve and muscle cells. [47] Ivermectin binding pushes these channels open, increasing the flow of chloride ions and hyper-polarizing the cell membranes. [47] [46] This hyperpolarization paralyzes the affected tissue, eventually killing the invertebrate. [47] In mammals (including humans) glutamate-gated chloride channels are restricted to the brain and spinal cord ivermectin cannot cross the blood-brain barrier and so it does not make it to the brain to affect mammalian channels. [47]


Ivermectin can be given by mouth, topically, or via injection. It does not readily cross the blood–brain barrier of mammals due to the presence of P-glycoprotein [48] (the MDR1 gene mutation affects function of this protein). Crossing may still become significant if ivermectin is given at high doses (in which case, brain levels peak 2–5 hours after administration). In contrast to mammals, ivermectin can cross the blood–brain barrier in tortoises, often with fatal consequences.


Field studies have demonstrated the dung of animals treated with ivermectin supports a significantly reduced diversity of invertebrates, and the dung persists longer. [49]

Fermentation of Streptomyces avermitilis yields eight closely related avermectin homologues, of which B1a and B1b form the bulk of the products isolated. In a separate chemical step, the mixture is hydrogenated to give ivermectin, which is an approximately 80:20 mixture of the two 22,23-dihydroavermectin compounds. [50] [51] [52]

The avermectin family of compounds was discovered by Satoshi Ōmura of Kitasato University and William Campbell of Merck. In 1970, Ōmura isolated unusual Streptomyces bacteria from the soil near a golf course along the south east coast of Honshu, Japan. [52] Ōmura sent the bacteria to William Campbell, who showed that the bacterial culture could cure mice infected with the roundworm Heligmosomoides polygyrus. [52] Campbell isolated the active compounds from the bacterial culture, naming them "avermectins" and the bacterium Streptomyces avermitilis for the compounds' ability to clear mice of worms (in Latin: a 'without', vermis 'worms'). [52] Of the various avermectins, Campbell's group found the compound "avermectin B1" to be the most potent when taken orally. [52] They synthesized modified forms of avermectin B1 to improve its pharmaceutical properties, eventually choosing a mixture of at least 80% 22,23-dihydroavermectin B1a and up to 20% 22,23-dihydroavermectin B1b, a combination they called "ivermectin". [52] [53]

Ivermectin was introduced in 1981. [54] Half of the 2015 Nobel Prize in Physiology or Medicine was awarded jointly to Campbell and Ōmura for discovering avermectin, "the derivatives of which have radically lowered the incidence of river blindness and lymphatic filariasis, as well as showing efficacy against an expanding number of other parasitic diseases". [55]

The initial price proposed by Merck in 1987 was US$6 per treatment, not affordable for most patients in Africa. [56] The company donated hundreds of millions of courses of treatments since 1988 in more than 30 countries. [56] Between 1995 and 2010 the program using donated ivermectin to prevent river blindness is estimated to have prevented seven million years of disability whilst costing US$257 million. [57]

As of 2019 [update] , the cost effectiveness of treating scabies and lice with ivermectin has not been studied. [58] [59]

As of 2019, ivermectin tablets in the United States were the least expensive treatment option for lice in children at about US$10 . [60] The hair lotion, however, costs [ which? ] about US$300 for a course of treatment. [60]

Brand names

Ivermectin is available as a generic prescription drug in the U.S. in a 3 mg tablet formulation. [61] It is also sold under the brand names Heartgard, Sklice [62] and Stromectol [63] in the United States, Ivomec worldwide by Merial Animal Health, Mectizan in Canada by Merck, Iver-DT [64] in Nepal by Alive Pharmaceutical and Ivexterm in Mexico by Valeant Pharmaceuticals International. In Thailand it is manufactured by Atlantic Laboratories [65] and sold as Vermectin. [66] In Southeast Asian countries, it is marketed by Delta Pharma Ltd. under the trade name Scabo 6. The formulation for rosacea treatment is sold as Soolantra. While in development, it was assigned the code MK-933 by Merck. [67]

COVID-19 misinformation

In December 2020, Chair of the US Senate Homeland Security Committee Ron Johnson used a Senate hearing to promote fringe theories about COVID-19. [68] Among the witnesses was Pierre Kory, a pulmonary and critical care doctor, who erroneously described ivermectin as "miraculous" and as a "wonder drug" to be used against COVID-19. Video footage of his statements went viral on social media, receiving over one million views as of 11 December. [69] In the United Kingdom Andrew Hill, a senior research fellow at Liverpool University, posted a video of a draft meta-analysis that went viral before it was removed. [70]

During the pandemic, a number of misleading websites appeared purporting to show meta-analyses of clinical evidence in favour of ivermectin and sporting colorful graphics. While these gained traction in social media they violated the necessary norms of scientific practice, and the misinformation they contained created confusion among the public and policy makers. [71]

A review article by Kory, Paul E. Marik, and others on the efficacy of ivermectin, which had been provisionally accepted for publication by a Frontiers Media journal, was subsequently rejected on account of what the publisher said were "a series of strong, unsupported claims based on studies with insufficient statistical significance" meaning that the article did "not offer an objective [or] balanced scientific contribution to the evaluation of ivermectin as a potential treatment for COVID-19". [72]

In the United States, the use of ivermectin for COVID-19 is championed by a group calling itself the "Frontline COVID-19 Critical Care Alliance" (FLCCC), which says it heads "the global movement to move #Ivermectin into the mainstream". The effort has gone viral on social media, where it has been adopted by COVID deniers, anti-vaccination proponents, and conspiracy theorists. [73] David Gorski has written that the narrative of ivermectin as a "miracle cure" for COVID-19 is a "metastasized" version of a similar conspiracy theory around the drug hydroxychloroquine, in which unspecified powers are thought to be suppressing news of the drug's effectiveness for their own profit. [74]

The viral social media misinformation about ivermectin has gained particular attention in South Africa where an anti-vaccination group called "South Africa Has A Right To Ivermectin" has been lobbying for the drug to be made available for prescription. [70] Another group, the "Ivermectin Interest Group" launched a court case against the South African Health Products Regulatory Authority (SAHPRA), and as a result a compassionate use exemption was granted. SAPHRA stated in April 2021 that "At present, there are no approved treatments for COVID-19 infections". [70]


In vitro, ivermectin has antiviral effects against several distinct positive-sense single-strand RNA viruses, including SARS-CoV-2. [75] Subsequent studies found that ivermectin could inhibit replication of SARS-CoV-2 in monkey kidney cell culture with an IC50 of 2.2–2.8 μM. [76] [77] Based on this information, however, doses much higher than the maximum approved or safely achievable for use in humans would be required for an antiviral effect. [78] [79] Aside from practical difficulties, such high doses are not covered by current human-use approvals of the drug and would be toxic, as the antiviral mechanism of action is considered to operate via the suppression of a host cellular process, [78] specifically the inhibition of nuclear transport by importin α/β1. [80] Therefore, the rationale for the clinical evaluation of ivermectin in COVID-19 seems insufficient. [81] Self-medication with a highly concentrated formula intended for horses has led to multiple hospitalizations, and overdose can lead to death, possibly due to interaction with other medications. [82] Additional evidence of safety and efficacy from RCTs and dose-response studies is needed. [83] At least 45 such trials were listed as of January 2021. [84]

Many studies on ivermectin for COVID-19 have serious methodological limitations, resulting in very low evidence certainty. [81] [85] As a result, several organizations have publicly expressed that the evidence of effectiveness against COVID-19 is weak. In February 2021, Merck, the developer of the drug, issued a statement saying that there is no good evidence ivermectin is plausible or effective against COVID-19, and that attempting such use may be unsafe. [86] [87] The U.S. National Institutes of Health COVID-19 Treatment Guidelines state that the evidence for ivermectin is too limited to allow for a recommendation for or against its use. [88] In the United Kingdom, the national COVID-19 Therapeutics Advisory Panel determined that the evidence base and plausibility of ivermectin as a COVID-19 treatment were insufficient to pursue further investigations. [89]

Ivermectin is not approved by the U.S. Food and Drug Administration (FDA) for anti-viral use [88] and is not authorized for use to treat COVID-19 within the European Union. [90] After reviewing the evidence on ivermectin, the EMA said that "the available data do not support its use for COVID-19 outside well-designed clinical trials". [90] In March 2021, both the FDA and the European Medicines Agency (EMA) issued guidance that ivermectin should not be used to treat or prevent COVID-19. [82] [90] The WHO also said that ivermectin should not be used to treat COVID-19 except in a clinical trial. [91] The Brazilian Health Regulatory Agency, Brazilian Society of Infectious Diseases, and Brazilian Thoracic Society issued position statements advising against the use of ivermectin for prevention or treatment of early-stage COVID-19. [92] [93] [94]

Misinformation, lower degrees of trust, a sense of loss of control and despair over the increase in the number of cases and deaths led to an increase in the use of the drug and the emergence of a black market in Central and Eastern Europe, Latin America [95] [96] and South Africa, raising concerns about self-medication, safety and feasibility of future clinical trials. [97] Despite the absence of high-quality evidence to suggest any efficacy and advice to the contrary, some governments have allowed its off-label use, including Czech Republic, [97] Slovakia, [97] Peru (later rescinded despite continuing use), [98] [99] and India. [100] [101]

Tropical diseases

Ivermectin is being studied as a potential antiviral agent against chikungunya and yellow fever. [102]

Ivermectin is also of interest in the prevention of malaria, as it is toxic to both the malaria plasmodium itself and the mosquitos that carry it. [103] [104] A direct effect on malaria parasites could not be shown in an experimental infection of volunteers with Plasmodium falciparum. [105] Use of ivermectin at higher doses necessary to control malaria is probably safe, though large clinical trials have not yet been done to definitively establish the efficacy and safety of ivermectin for prophylaxis or treatment of malaria. [106] Mass drug administration of a population with ivermectin for purposes of treating/preventing nematode infestation is effective for eliminating malaria-bearing mosquitos and thereby reducing infection with residual malaria parasites. [107]

Moxidectin has been approved by the FDA for use in people with river blindness, has a longer half-life than ivermectin, and may eventually supplant ivermectin, as it is a more potent microfilaricide, but there is a need for additional clinical trials, with long-term follow-up, to assess whether moxidectin is safe and effective for treatment of nematode infection in children and women of childbearing potential. [108] [109]

Bedbugs: There is tentative evidence that ivermectin kills bedbugs, as part of integrated pest management for bedbug infestations. [110] [111] [112] Such use however may require a prolonged course of treatment which is of unclear safety. [113]


In 2013, this antiparasitic drug was demonstrated as a novel ligand of farnesoid X receptor (FXR), [114] [115] a therapeutic target for nonalcoholic fatty liver disease. [116]

Ivermectin is routinely used to control parasitic worms in the gastrointestinal tract of ruminant animals. These parasites normally enter the animal when it is grazing, pass the bowel, and set and mature in the intestines, after which they produce eggs that leave the animal via its droppings and can infest new pastures. Ivermectin is effective in killing some, but not all, of these parasites. [ citation needed ]

In dogs it is routinely used as prophylaxis against heartworm. [117]

Dogs with defects in the P-glycoprotein gene (MDR1), often collie-like herding dogs, can be severely poisoned by ivermectin. The mnemonic "white feet, don't treat" refers to Scotch collies that are vulnerable to ivermectin. [118] Some other dog breeds (especially the Rough Collie, the Smooth Collie, the Shetland Sheepdog, and the Australian Shepherd), also have a high incidence of mutation within the MDR1 gene (coding for P-glycoprotein) and are sensitive to the toxic effects of ivermectin. [119] [120] Clinical evidence suggests kittens are susceptible to ivermectin toxicity. [121] A 0.01% ivermectin topical preparation for treating ear mites in cats is available. [122]

Ivermectin is sometimes used as an acaricide in reptiles, both by injection and as a diluted spray. While this works well in some cases, care must be taken, as several species of reptiles are very sensitive to ivermectin. Use in turtles is particularly contraindicated. [123]

Catch Nature!

Tell us what you think of our planned improvements for Willowbrook Wildlife Center so it can remain a national leader in wildlife rehabilitation.

It's the time of year when turtles take to the streets in search of nesting sites. Do your part by slowing down and watching for them when driving.

We all know which dads rate in humans, but ever wonder which dads are kings in native wildlife? Find out which pops are tops among DuPage wildlife.

Explore the impact glaciers had on this little-known section of Churchill Woods Forest Preserve and how it once provided railroad service to Chicago.

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Your Links to Nature

The Forest Preserve District of DuPage County offers scores of nature-related programs and activities for grownups, kids, families and groups year-round. Click below to register for programs, reserve shelters and campsites or purchase permits, and we'll see you soon!

Major Issues and Accomplishments

Religious Freedom: Defeated a proposed county zoning ordinance that would have prohibited places of worship from building or expanding in residential areas. Also won a long battle for county board approval to build a mosque in Willowbrook after repeated denials for a zoning variance.

Education/Immigration: Protected and expanded tuition-free English as a Second Language (ESL) courses at College of DuPage, impacting more than 2000 students.

Government Reform: Identified financial mismanagement of a government entity, the DuPage Water Commission (DWC). Was instrumental is passing two state laws. The first stripped DWC of a 1/4 cent sales tax beginning in 2016, saving taxpayers $35 million a year and eliminating a regressive tax that falls disproportionately on low-income residents. The second adds transparency to appointed commissions by requiring those appointed by county boards to submit financial, personnel and contract documentation.

Workforce Development: Leveraged a commitment of $200,000 from DuPage County to support a pilot project connecting good people to good jobs. DuPage United launched Career Connect Metro West to recruit candidates for two established organizations that were ready link those prospects to needed resources, train them and place them into existing unfilled good-paying jobs. The ability of Career Connect to recruit unemployed and underemployed candidates from our own institutional members and from other non-profits greatly exceeded the ability of the partners to train and place those candidates. The pilot program will be evaluated and revamped going forward and additional training/placement partners sought.

County Safety Net: Took the lead in getting funding reinstated for the DuPage County Human Service Grants Fund every year since 2008. This has provided over $7 million to non-profits to assist with food, shelter, and other basic needs.

Awards: Received the Interfaith Unity Award from the Islamic Society of North America and the United Methodist Bishops' Award for Ecumenical and Interfaith Work.

Foundation Established

In an effort to recognize the growing need to create accessible play for DuPage County children with autism, the Play For All Garden & Playground Foundation was established. The Foundation is represented by an array of accessibility and recreation experts that includes the Wheaton Park District, Western DuPage Special Recreation Association, Forest Preserve District of DuPage County, Shane’s Inspiration, Landscape Structures, and Kiwanis Club of Wheaton.

As a primary initiative of the Foundation, the group is committed to developing the Sensory Garden Playground – a free of charge facility that brings together the benefits of gardens and playgrounds with other necessary amenities in a welcoming, accessible, and safe environment where abilities can be developed and an appreciation for each other’s differences are embraced for all children.


DuPage County Historical Museum Mission

The DuPage County Historical Museum is operated as a facility of Wheaton Park District, owned by the County of DuPage by resolution of the County Board pursuant to state statute. Its principal purposes are to educate the general public through the collection, preservation, interpretation, and exhibition of materials which document the history of DuPage County and its relationship to Illinois and the nation, and to provide local history services for historical organizations and for scholarly endeavors.

Wheaton Park District Vision

We, the Wheaton Park District team, commit to service excellence, financial stability and an enriched quality of life for our stakeholders. We accomplish this through continuous improvement of people and systems while living our values.

Why donate to the DuPage County Historical Museum?

With your donation you become a steward of your own history. You help to preserve your community’s historical and cultural identity. You are educating the 10,000+ people who come through the museum doors or participate in events every year. You are engaging the community with the stories of their past and providing a safe and inclusive place to discuss these topics.

Will you preserve your history by making a donation to the DuPage County Historical Museum?

1960sBuilt With Innovation

DuPage Med­ical Group began 50 years ago as the brain­child of Dr. Robert McCray, a local sur­geon and health care vision­ary. Dr. McCray’s advance­ments helped rede­fine the physi­cian prac­tice in DuPage Coun­ty into the kind of per­son­al­ized, lead­ing-edge health care that until then was rarely avail­able out­side the uni­ver­si­ty med­ical or research cen­ter settings.

In the ear­ly 1960s, Dr. McCray vis­it­ed 35 US clin­ics, includ­ing Minnesota’s Mayo Clin­ic, exam­in­ing ele­ments that made group prac­tices suc­cess­ful. He teamed with sev­er­al physi­cians – fel­low sur­geon and part­ner Dr. Glen Asselmeier, internists Drs. Joe Crum­rine, Fred Kuharich and James Erlen­born and pedi­a­tri­cians Drs. James Ver­coe and William Kin­dra­chuk. Dr. Gary Chris­tensen joined the team after com­plet­ing a res­i­den­cy in obstet­rics and gynecology.

The group broke ground in August 1963 on a 12,000-square-foot build­ing. They named the clin­ic Glen Ellyn Clin­ic, part­ly in homage to the Mayo Clinic.

Glen Ellyn Clin­ic opened on Sep­tem­ber 1, 1964, with eight physi­cians, 15 nurs­es and a staff of lab tech­ni­cians and admin­is­tra­tive per­son­nel. The clin­ic offered ground­break­ing inno­va­tions for its time – a lab­o­ra­to­ry, X‑ray ser­vices and a phar­ma­cy, all onsite.

1970sSuc­cess and Growth

By 1970, the part­ner­ship had 25 physi­cians see­ing more than 300 new patients a month. Office and lab space was added thanks to a 24,000-square-foot expansion.

Growth con­tin­ued in the ear­ly 1970s. Two new office build­ings accom­mo­dat­ed new med­ical spe­cial­ists. New physi­cians saw Glen Ellyn Clin­ic as an oppor­tu­ni­ty to prac­tice in the com­pa­ny of estab­lished col­leagues. The clin­ic also intro­duced a range of spe­cial­ties to the West­ern Sub­urbs, includ­ing tho­racic surgery, neu­ro­surgery, car­diac surgery, gas­troen­terol­o­gy, inva­sive car­di­ol­o­gy and neonatology.

1980sCon­tin­ued Expansion

In the 1980s, the clin­ic added 38,000 square feet of office and lab space to accom­mo­date physi­cians in 16 spe­cial­ties and sub-spe­cial­ties. Clin­ic offices were opened in Bloom­ing­dale and Naperville. By the end of the decade, the Glen Ellyn Clin­ic was one of the city’s largest employ­ers – 80 physi­cians and 480 staff han­dled 300,000 annu­al patient vis­its. It also owned one of the largest clin­ic-oper­at­ed labs in Illi­nois, per­form­ing more than 100,000 tests onsite and 25,000 more off­site every year.

1990sChange and Transition

In the 1990s, the clin­ic joined the country’s largest physi­cian man­age­ment com­pa­ny to ensure the finan­cial strength it need­ed to con­tin­ue growing.

As man­aged care gained ground in the 1990s, physi­cian groups across the coun­try expe­ri­enced increas­ing pres­sures, includ­ing two oth­ers in DuPage Coun­ty that would fig­ure promi­nent­ly in the Glen Ellyn Clinic’s future – Mid-Amer­i­ca Health Part­ners and Wheaton Med­ical Clinic.

Wheaton Med­ical Clin­ic includ­ed 25 physi­cians and had recent­ly affil­i­at­ed itself with a major health insur­er, and Mid-Amer­i­ca Health Part­ners’ 50 pri­ma­ry care physi­cians had formed in 1995 as a physi­cian-led inde­pen­dent prac­tice group. After Wheaton Med­ical Clin­ic merged with the Glen Ellyn Clin­ic in 1997, Mid-Amer­i­ca joined the fol­low­ing year. Short­ly after, physi­cians from all three began efforts to return the com­bined clin­ic to the pri­vate physi­cian group-prac­tice mod­el under local control.

The result was DuPage Med­ical Group, which was formed in 1999.

TodayCom­mit­ment to the Road Ahead

DuPage Med­ical Group is now the state’s lead­ing mul­ti-spe­cial­ty group prac­tice. DuPage Med­ical Group is still com­mit­ted to supe­ri­or care and inno­va­tion, with a lead­er­ship struc­ture designed to main­tain bal­ance between pri­ma­ry and spe­cial­ty care. With near­ly 600 pri­ma­ry care and spe­cial­ty physi­cians in more than 70 loca­tions, DuPage Med­ical Group han­dles upwards of 1.1 mil­lion patient vis­its annu­al­ly, treat­ing about a third of DuPage County’s population.

Today, DuPage Med­ical Group is expe­ri­enc­ing unprece­dent­ed growth and expan­sion into neigh­bor­ing coun­ties as the orga­ni­za­tion con­tin­u­ous­ly strives to meet pop­u­la­tion growth and move­ment. Car­ry­ing on the lega­cy of Dr. McCray and his co-founders, DuPage Med­ical Group is focused on pro­vid­ing the West­ern Sub­urbs with access to the finest health care avail­able and oper­at­ing on the prin­ci­ple that physi­cians make the best deci­sions for patient care.

Watch the video: 2021 APA Visionaries Short Film Competition. HBO


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    the very good idea

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