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« Last post by smfadmin on December 21, 2025, 03:36:17 PM »
⚖️ Comprehensive Harm‑Reduction Overview: Stopping Clopixol Depot (Zuclopenthixol Decanoate) PurposeThis post compiles general patterns reported by individuals who discontinue a long‑acting antipsychotic depot. It is descriptive, not prescriptive. Experiences vary widely depending on dose, duration, metabolism, stress load, and individual neurochemistry. ✅ Potential Benefits of Discontinuation1. Reduced Sedation & Cognitive Drag- Less daytime fatigue
- Sharper cognition and faster processing
- Improved reaction time
- Better initiative and drive
2. Reduction in Extrapyramidal Symptoms (EPS)- Less rigidity or stiffness
- Reduced tremor
- Less akathisia
- Improved motor fluidity
3. Emotional “Unflattening”- More emotional range
- Less blunting
- Improved libido
- Better reward sensitivity and motivation
4. Increased Autonomy & Self‑Management- No depot appointments
- More control over neurochemistry
- Ability to fine‑tune personal regimen based on lived experience
5. Reduced Pharmacological Load- Lower anticholinergic burden
- Reduced metabolic drag
- Less prolactin elevation
- Lower cardiovascular strain
⚠️ Risks of Discontinuation1. Return of Underlying Symptoms- Psychosis
- Paranoia
- Agitation
- Sleep disruption
- Disorganized or intrusive thinking
Note: Depot fade is slow. Relapse can occur 2–8 weeks after the last injection.2. Rebound / Withdrawal‑Like Effects- Anxiety
- Restlessness
- Insomnia
- Irritability
- Transient dysphoria
3. Withdrawal Dyskinesia (Uncommon)- Involuntary movements
- Facial/tongue movements
- Typically temporary
4. Loss of Protective Buffer- Reduced mood stabilization
- Loss of anti‑agitation effect
- No antipsychotic coverage during stressors
5. Increased Sensitivity to Other Substances- Stimulants may feel stronger
- GABAergic rebound may be more pronounced
- THC can become destabilizing
🧠 Neutral / Individual‑Dependent Factors- Sleep quality
- Appetite
- Stress tolerance
- Emotional intensity
- Impulse control
🗓️ Timeline: Commonly Reported Patterns After Stopping a DepotWeek 0–1: Immediate Post‑Depot Period- Depot still active; plasma levels decline slowly.
- Most people feel no major change yet.
- Sedation, EPS, and emotional blunting remain largely unchanged.
- Some report subtle increases in alertness or energy.
Week 2–3: Early Fade Phase- Sedation may begin to lighten.
- Cognitive clarity may improve slightly.
- EPS (if present) may start to ease.
- Some individuals report mild restlessness or sleep changes.
- Underlying symptoms typically remain stable due to residual depot effect.
Week 4–5: Mid‑Fade Window- Noticeable reduction in sedation for many.
- Emotional range may increase (“unflattening”).
- Motor side‑effects often continue improving.
- Some may experience transient anxiety, irritability, or sleep disruption as dopamine blockade decreases.
- This is often the earliest point where underlying symptoms may begin to re‑emerge in sensitive individuals.
Week 6–8: Late Fade / Vulnerability Window- Depot effect significantly reduced.
- Cognitive sharpness and motivation may increase further.
- Emotional intensity may feel stronger — positive or negative.
- Some individuals report rebound‑type effects (restlessness, insomnia, agitation).
- This is the period where relapse risk is typically highest if underlying symptoms were previously controlled by the depot.
- Rarely, withdrawal dyskinesia may appear as dopamine receptors re‑sensitize.
Week 9–12: Post‑Depot Baseline Emerges- Most or all pharmacological effect has worn off.
- Side‑effects (sedation, EPS, blunting) are usually minimal or gone.
- Neurochemistry stabilizes into a new baseline.
- Underlying symptoms — if they return — often do so in this window.
- Sensitivity to stimulants, THC, and GABAergic agents may be higher than before.
3 Months and Beyond- Long‑term baseline becomes clearer.
- Some individuals feel significantly better without the depot.
- Others may experience recurring symptoms depending on stress load and personal history.
- Motor and cognitive improvements (if any) tend to plateau.
📌 Summary (SMF‑Compatible Header Simulation)Cognition- Benefit: Sharper, less sedated
- Risk: Possible agitation or insomnia
Motor System- Benefit: Less EPS
- Risk: Withdrawal dyskinesia (rare)
Emotion- Benefit: More range, less blunting
- Risk: Mood instability
Psychosis Risk- Benefit: —
- Risk: Relapse risk increases
Autonomy- Benefit: Full control
- Risk: Loss of safety buffer
Pharmacology- Benefit: Reduced anticholinergic load
- Risk: Dopamine rebound effects
Notes- Depot pharmacokinetics vary; some people metabolize faster or slower.
- Stress, sleep, substance use, and environment strongly influence outcomes.
- This post is descriptive, not advisory.
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« Last post by smfadmin on December 19, 2025, 10:39:35 AM »
RELATIONSHIPS:
1. No man wants a woman who is accessible to every man.
2. You will reach the age where you can easily tell that the relationship is not going to work just by the conversation.
3. If you have to beg someone to do the bare minimum for you and if you have to keep telling them how you deserved to be treated better then for goodness sake. LEAVE. It's not worth your peace.
4. Don’t ignore the red flags you see at the beginning. The red flags you ignore trying to see the good in people WILL cost you later.
5. Just because a person keeps you around doesn’t mean they love you; remember, people, buy cats just to get rid of rats.
6. If SEX is all you are about in a relationship, then it means you are actually empty. A healthy relationship is about purpose! Sharing visions and values together.
7. In life, you need to learn to stop opening doors for toxic people and giving them room in your mind, and calling it "seeking closure!" You're delaying your healing process.
8. Avoid the damaged, the unhappy, and the unlucky.
9. Anger opens the mouth and shuts the mind. Control your. Anger so that you can think fast and get solution to what cause your anger
10. As a woman, understand that men will say and do anything to sleep with you. Look at the actions, don’t be blinded by words. Anyone can talk a good game, but it takes a real ball player to play.
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« Last post by Chip on December 19, 2025, 04:39:21 AM »
Urine Drug Testing – Cocaine & Methamphetamine (MA)
Scope
This page covers typical urine detection windows for cocaine and methamphetamine (MA), including chronic-use scenarios. Times assume standard lab immunoassay cut-offs.
Cocaine
What is detected:
• Benzoylecgonine (main metabolite)
• Cocaine itself clears very fast
Detection window (urine):
• Single / occasional use: 2–3 days
• Heavy or repeated use: 5–7 days
• Extreme binges (rare): up to 10–14 days
Notes:
• Cocaine has one primary metabolite
• Short-lived compared to stimulants like MA
• Most users are clear within 72 hours
Methamphetamine (MA)
What is detected:
• Methamphetamine
• Amphetamine (active metabolite – this is the limiter)
Detection window (urine):
• Single / light use: 2–4 days
• One-day heavy use: 4–6 days
• Multi-day binge (2–4 days): 6–8 days
• Chronic / high-dose use: 8–10 days
• Outliers (daily, long-term use): up to 14 days
Why MA lasts longer than cocaine:
• Converts to amphetamine
• Amphetamine accumulates with repeated use
• Chronic use causes metabolite stacking
Route of Use
• IV / smoked: slightly longer tail
• Nasal: middle
• Oral: slightly shorter
Frequency and total dose matter far more than route
Urine pH & Hydration
• Alkaline urine = slower excretion
• Acidic urine = faster excretion
• Labs account for dilution; hydration does not “cheat” tests
Rule of Thumb
• Cocaine: usually clear in ≤3 days
• MA single use: ~3–4 days
• MA binge: ~7 days
• MA chronic: 10+ days possible
Important:
Long detection times are driven by chronic daily use without breaks, not isolated doses.
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« Last post by Chip on December 09, 2025, 10:16:21 AM »
https://www.wired.com/story/a-fentanyl-vaccine-is-about-to-get-its-first-major-test/?utm_source=nl&utm_brand=wired&utm_mailing=WIR_Science_120825&utm_campaign=aud-dev&utm_medium=email&utm_term=WIR_Science&utm_content=WIR_Science_120825&bxid=67883001cdeb6340250c3d97&cndid=85787720&hasha=c9edd795ab58c731e64cc2832451a46d&hashb=92cd5a4e4f9a554757364e6cc6a52d8ff33f14ec&hashc=1e7f7a9239bb44f191dc979b8fe5e634e587dfe020b84a653d2040468a8b342b&esrc=bx_multi1st_science* There is an audio file available at the link A Fentanyl Vaccine Is About to Get Its First Major TestDec 3, 2025 ARMR Sciences of New York is trialing a vaccine in the Netherlands to protect against fentanyl-related overdose and death. Just a tiny amount of fentanyl, the equivalent of a few grains of sand, is enough to stop a person’s breathing. The synthetic opioid is tasteless, odorless, and invisible when mixed with other substances, and drug users are often unaware of its presence. PHOTO-ILLUSTRATION: WIRED STAFF; GETTY IMAGES:
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« Last post by Chip on December 07, 2025, 09:27:29 AM »
https://neurosciencenews.com/episodic-memory-change-30022/Why Memories Change: How the Brain Rewrites the PastDecember 5, 2025 Summary: A new review explores how episodic memories are formed, stored, and reshaped over time, revealing why our recollections of past events often change. Rather than functioning like fixed files, memories consist of multiple components that can lie dormant until triggered by environmental cues. When retrieved, these components blend with general knowledge, past experiences, and current context, creating updated versions of the original event. The findings help explain memory distortion and offer insights for mental health, learning, and legal settings where accuracy matters. Neuroscience News logo for mobile. This shows a head and a brain. A key part of the study focused on how the brain physically stores memories, highlighting the role of the hippocampus - a part of the brain that helps form and organise memories. Credit: Neuroscience News Why Memories Change: How the Brain Rewrites the Past FeaturedNeuroscience·December 5, 2025 Summary: A new review explores how episodic memories are formed, stored, and reshaped over time, revealing why our recollections of past events often change. Rather than functioning like fixed files, memories consist of multiple components that can lie dormant until triggered by environmental cues. When retrieved, these components blend with general knowledge, past experiences, and current context, creating updated versions of the original event. The findings help explain memory distortion and offer insights for mental health, learning, and legal settings where accuracy matters. Key Facts * Dynamic Memories: Episodic memories are continually updated, not stored as perfect copies. * Trigger-Based Recall: Hidden memory traces become conscious only when activated by cues. * Real-World Impact: Memory reshaping affects mental health, education, and legal decision-making. Source: University of East Anglia A study from the University of East Anglia is helping scientists better understand how our brains remember past events – and how those memories can change over time. A new paper published today explores episodic memory – the kind of memory we use to recall personal experiences like a birthday party or a holiday. The team say their work has important implications for mental health, education, and legal settings where memory plays a key role. The article continues at the source link above ...
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« Last post by smfadmin on December 04, 2025, 01:53:58 PM »
1,4-Butanediol (1,4-BDO) / GHB Overview and Urine-Analysis
Key Points:- 1,4-BDO is metabolized in the body into GHB.
- Urine tests usually detect GHB, not 1,4-BDO itself.
- Detection times are short due to rapid metabolism.
Detection Windows| [th]Sample Type[/th][th]Detection Window[/th][th]Notes[/th] | | Urine (standard test) | ~6–12 hours | Most standard tests detect GHB shortly after use. | | Urine (sensitive forensic tests) | Up to 24 hours | Highly sensitive labs may detect metabolites longer. | | Blood / Plasma | ~1–4 hours | Very short; rapid metabolism to GHB. | | Hair | Up to 90 days | Can detect repeated or chronic use; single use detection less reliable. |
Urine Clearance Timeline (Approximate)Time after ingestion → Likely Detection in Urine
0–2 hrs █████████████ Very high (recent use)
2–6 hrs ████████ High
6–12 hrs ████ Moderate → Low
12–24 hrs ██ Low → Rare
>24 hrs ░ Usually undetectable
Effects of 1,4-BDO (Conceptual, Tolerance Considered)| [th]1,4-BDO Dose (mL)[/th][th]GHB Equivalent (g)[/th][th]Naïve User Effects[/th][th]High-Tolerance User Effects[/th][th]Risk Level[/th] | | 1–2 | 0.6–1.2 | Mild euphoria, relaxation, light sedation | Mild relaxation, slight euphoria | Low | | 3–4 | 1.8–2.4 | Strong euphoria, impaired coordination, nausea | Euphoria, relaxation, moderate sedation | Moderate | | 5–6 | 3–3.6 | Heavy sedation, risk of vomiting, blackouts | Strong euphoria, sedation, impaired motor skills | High | | 6.8 | ~4.1 | Very strong sedation, high risk of unconsciousness, vomiting, respiratory depression | Strong sedation, euphoria, risk of blackouts, still significant overdose potential | Very High | | 7–8 | 4.2–4.8 | Life-threatening overdose | Severe sedation, risk of unconsciousness, respiratory depression | Critical |
Conceptual Risk Pattern (Traffic-Light System)🟢 LOW | Light psychoactive effects possible. Function mostly intact.
🟡 MODERATE | Clear intoxication. Impaired coordination, sedation. Judgment reduced. Higher chance of vomiting or blackouts.
🟠 HIGH | Heavy sedation. Major impairment, possible amnesia. Sleep-like states, difficult to wake. Danger increases massively with any combo (alcohol, benzos, opioids).
🔴 VERY HIGH | High risk of overdose. Loss of consciousness, irregular breathing. Vomiting while unconscious possible. Risk of respiratory depression.
⚫ CRITICAL | Severe overdose range. Slow or stopped breathing. Medical emergency—risk of coma or death.
Important Safety Notes- Even high-tolerance users remain at serious risk at higher doses.
- Effects onset: ~15–30 min, peak ~45–90 min, duration 2–4 h.
- Mixing with alcohol or other depressants greatly increases risk.
- Tolerance does not prevent respiratory depression or overdose.
Disclaimer: This post is for informational purposes only and does not provide instructions for use. 1,4-BDO/GHB use carries significant risk of serious injury or death.
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« Last post by smfadmin on December 04, 2025, 01:29:57 AM »
https://www.psychiatrist.com/jcp/brexpiprazole-co-occurring-schizophrenia-substance-use-disorder-randomized-controlled-trial/?utm_source=Klaviyo&utm_medium=email&utm_campaign=news_wmr&klid=01HYSTTNXNB74YAYKT9XMYQCN0&_kx=va3uRF3O8-7Dg_zjrKMZJk0wdery-TOTVyZ3l8muM1g.VpkqxCBrexpiprazole for the Treatment of Co-occurring Schizophrenia and Substance Use Disorder: A Multisite, Randomized, Controlled TrialOctober 13, 2025 Abstract Objective: This proof-of-concept study examined the effects of brexpiprazole treatment on substance use, psychiatric symptoms, and quality of life in patients with co-occurring schizophrenia and substance use disorder. Methods: In this 12-week study, patients diagnosed with schizophrenia and substance use disorder using DSM-5 criteria were randomly assigned to switch from their current antipsychotic medication to brexpiprazole (up to 4 mg/day) or remain on their current antipsychotic treatment (treatment as usual [TAU]). Substance use was assessed by the number of days of substance use and the dollars spent on substance in the past week, and substance craving was assessed using the Visual Analog Scale (VAS). Quality of life was assessed using the Heinrichs-Carpenter Quality of Life Scale (QOL). In addition, psychiatric symptoms were assessed using the Positive and Negative Syndrome Scale (PANSS) and the Clinical Global Impression Scale-Severity of Illness. Results: Thirty-nine patients were randomized (21 in the brexpiprazole group, 18 in the TAU group). Mixed models for repeated measures showed that, despite the lack of statistical significance, a consistent pattern of decrease in the brexpiprazole group was observed for the number of days of substance use and the dollars spent, as well as substance craving; the brexpiprazole group had a 15.5 points greater decrease in VAS (P=.157) and a $33.3 greater decrease in the dollars spent (P=.108) from baseline to week 12 compared with the TAU group. The brexpiprazole group did show a statistically significant 8.9 points greater increase in QOL compared with the TAU group (P =.020). Even though it was not statistically significant, the brexpiprazole group had a 2.4-point greater decrease in the PANSS General Psychopathology subscale score (P=.150) and a 1.9-point greater decrease in the PANSS Negative Symptom subscale score (P=.126) compared with the TAU group. Conclusion: This study suggests that brexpiprazole might be beneficial in reducing substance craving and use in patients with schizophrenia and co-occurring substance use disorder; this potential benefit may help improve quality of life and overall psychiatric symptoms in a difficult-to-treat patient population.
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« Last post by Chip on December 02, 2025, 01:59:22 PM »
Comprehensive Summary: Pharmacodynamics & Pharmacokinetics of Phenazolam (Clobromazolam)
Abstract
Phenazolam (clobromazolam) is a triazolobenzodiazepine derivative of phenazepam, notable for its extraordinary potency.
- Computational QSAR models predict exceptionally strong binding to GABAa receptors, with subnanomolar Ki values (~0.2 nM for α1 and α5).
- This translates into pronounced sedative and amnesic effects at very low doses.
- Pharmacokinetically, the compound undergoes extensive metabolism via hydroxylation and glucuronidation, mediated by CYP3A4 and UGT enzymes.
- While absorption and renal excretion are inferred, precise parameters such as half-life and clearance remain undefined.
- The absence of direct physiological data underscores both its potential risks in illicit use and the urgent need for further experimental validation.
Background
Phenazepam, developed in the Soviet Union in the 1970s, is known for its long-lasting CNS depression and abuse potential.
Phenazolam modifies this scaffold by adding a triazole ring, a structural feature shared with alprazolam and triazolam, which enhances potency.
Unlike clinically established benzodiazepines, phenazolam remains a research chemical, with most of its properties inferred from analogs and computational models rather than direct studies.
Pharmacodynamics
Phenazolam acts as a positive allosteric modulator of the GABAa receptor.
- It enhances the inhibitory action of GABA by increasing chloride channel opening frequency.
- QSAR analysis yields a binding affinity (log 1/c = 10.14), surpassing flunitrazolam (8.88) and slightly higher than flualprazolam (10.13).
- Subunit selectivity favors α1 (sedation, amnesia) and α5 (memory impairment), with Ki values in the subnanomolar range.
- Predicted clinical effects: profound sedation, muscle relaxation, and amnesia, with comparatively weaker anxiolytic properties.
This makes phenazolam one of the most potent designer benzodiazepines currently identified.
Pharmacokinetics
Phenazolam undergoes complex metabolism:
- Phase I: Hydroxylation produces α-hydroxy, 4-hydroxy, and α-4-dihydroxy metabolites, primarily via CYP3A4.
- Phase II: Glucuronidation yields five conjugates (N-glucuronide, O-glucuronides, and dihydroxy glucuronides), catalyzed by UGT enzymes.
- Early metabolites appear within 60 minutes; late-phase metabolites emerge after 360 minutes.
- Renal excretion is the main elimination pathway, with metabolites detectable in urine, useful for forensic screening.
- Critical pharmacokinetic parameters (absorption rate, volume of distribution, half-life, clearance) remain unknown, leaving major data gaps.
Atomic Composition
The molecular breakdown of phenazolam highlights its pharmacological features:
- Carbon (C): 48.57%
- Hydrogen (H): 34.29%
- Nitrogen (N): 11.43%
- Chlorine (Cl): 2.86%
- Bromine (Br): 2.86%
Halogens (Cl + Br) together account for 5.71%, a small fraction that nonetheless significantly influences potency, metabolic stability, and duration of action.
Nitrogen content (11.43%) is critical for receptor binding and pharmacological activity.
Discussion
Phenazolam’s potency is driven by its halogenation and triazole ring.
- For researchers: these features warrant investigation into receptor binding, metabolism, and toxicity.
- For recreational users: the same features explain its strength and prolonged effects, but also raise risks of oversedation, respiratory depression, dependence, and cognitive decline.
- Even minor atomic contributions (like halogens at 5.71%) can drastically alter pharmacological behavior.
This duality—scientific intrigue vs. recreational hazard—defines phenazolam’s profile.
Conclusion
Phenazolam is a highly potent triazolobenzodiazepine with complex metabolism and strong receptor binding.
- Its predicted pharmacological profile emphasizes sedation and amnesia.
- Extensive hydroxylation and glucuronidation distinguish it from other triazolobenzodiazepines.
- Major data gaps remain, particularly regarding half-life, clearance, and dose-response in humans.
- Further experimental studies are essential to clarify its safety, therapeutic potential, and risks in illicit contexts.
Until such data are available, caution is strongly advised in both research and recreational settings.
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« Last post by Chip on December 02, 2025, 05:41:59 AM »
https://neurosciencenews.com/insomnia-circadian-dysfunction-29996/Insomnia (and Meth?) Keeps the Brain Stuck in Daytime Mode(Editor: Methamphetamine also causes Insomnia) December 1, 2025 Summary: People with chronic insomnia show a delayed and weakened daily rhythm of mental activity, keeping the brain in a more alert, daytime-like state at night. Under tightly controlled conditions, individuals with insomnia failed to show the normal nighttime drop in goal-directed thinking seen in healthy sleepers. Their peak cognitive activity also shifted roughly six and a half hours later than normal. These findings suggest insomnia involves a biological timing problem in how the brain powers down, not just behavioral difficulty falling asleep. Key Facts ● Circadian Shift: Mental activity peaks occur hours later in people with insomnia. ● Blunted Nighttime Shutdown: The expected drop in cognitive engagement during night is reduced. ● Treatment Implications: Strengthening circadian rhythms may improve sleep outcomes. Source: University of South Australia Australian researchers have found compelling evidence that insomnia may be linked to disruptions in the brain’s natural 24-hour rhythm of mental activity, shedding light on why some people struggle to ‘switch off’ at night. Published in Sleep Medicine, the study led by the University of South Australia (UniSA) is the first to map how cognitive activity fluctuates across the day in individuals with chronic insomnia, compared to healthy sleepers. The article continues at the link at the top ...
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« Last post by smfadmin on December 02, 2025, 05:36:19 AM »
https://www.popularmechanics.com/technology/a69459642/wukong-monkey-brain-neuromorphic-supercomputer/?source=nl&utm_source=nl_pop&utm_medium=email&date=112925&utm_campaign=nl01_112925_HBU42739672&oo=&user_email=1e7f7a9239bb44f191dc979b8fe5e634e587dfe020b84a653d2040468a8b342b&GID=1e7f7a9239bb44f191dc979b8fe5e634e587dfe020b84a653d2040468a8b342b&utm_term=Pop%20Mech%20Flagship%20Sending%20AudienceChina Claims It Uploaded a Monkey Brain to a Supercomputer—Possibly Bringing Us Closer to the SingularityNov 19, 2025 11:34 AM If this neuromorphic machine is real, it’s a milestone for neuroscience—and a test of what AI can and can’t replace. Researchers in China recently made an astonishing announcement: They’d created a supercomputer modeled on a monkey’s brain. Researchers at the National Key Laboratory of Brain-Computer Intelligence at Zhejiang University dubbed the supercomputer Darwin Monkey, or “Wukong,” after the mythological primate that was one of the chief inspirations behind the Dragon Ball Z character, Goku. The scientists designed their machine to mimic the brain of a macaque, a type of monkey often used in scientific research, because it exhibits human-like intelligence and cognition, according to a university press release originally written in Chinese and translated into English. They say it’s “a step toward more advanced brain-like intelligence.” Wukong consists of over two billion spiking neurons in an artificial neural network, which imitate biological neurons by communicating with each other through electrical pulses referred to as spikes. The supercomputer also includes 100 billion synapses, or the area where two neurons connect, allowing them to “communicate” with each other by passing a signal back and forth. That makes Wukong potentially the largest neuromorphic, or brain-like, computer in the world. Because these machines mimic biological circuitry, they’re highly energy efficient. Traditional supercomputers torch through multiple megawatts of power; meanwhile, Wukong is able to run on about 2,000 watts, not dissimilar from a household appliance. The article continues at the source link at the top of the page ...
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