Can Hydrogen Peroxide Cause Death?

I've heard of Oxygen Therapy, but nothing could convince me to drink the stuff other than swishing it around for whiter teeth or a cut. When I had a medical difficulty, I started to put cosmetic grade peroxide in my bath water (at the risk of looking real weird, I will admit this was from high strength hair color developers found in beauty supply stores, and I still question the safety of that.. but afterall it is understood to be on the skin at lengths of time. . not that I trust the ingredients in a lot of products that are allowed for the skin). I think that people tend to underestimate the power of skin absorption. A little fizzy kind of. I did think I got a little energy buzz from it, but at the same time, I think there was a tendency to conk out and sleep afterwards.

Can Hydrogen Peroxide Cause Death? 1

1. Is ist possible for death to occur due to over admistered oxygen therapy; at night for instance?

Depending on the liter flow. Some COPDers can only handle 2 liters of O2. While others can handle more. Find out what is the best amount of liters of O2 that he can handle. One that gives him a good sat and does not make him feel bad. A way to tell if he is getting to much O2 or if the liter flow is too high, is if he becomes drowsy and incoherent. Too much O2 flow can knock a COPDers drive to breathe and will make them sleepy and not want to breathe. The bad effects of O2 come from the liter flow and not how long they have it on. He can have it on all day and be fine but if you increase the liter flow too much it can make him sick

2. COVID-19: How 'Oxygen-at-Home' via Concentrators Can Be a Life Saver

On April 19, Nagpur-based Simran Nashine logged into her Twitter account to seek help for 41-year-old Girish Kesai, a COVID-19 patient. His oxygen saturation levels had dropped to 82%. It had been well over 24 hours since his health had started deteriorating, and the wait for a hospital bed with an oxygen facility was only increasing. Fortunately, within the next few hours, Girish was able to receive admission. In those critical hours between his oxygen levels dropping and him finally being admitted to the hospital, his life depended on an oxygen concentrator. This machine filters oxygen from the atmosphere and helps patients access it through a mask or cannula. "The machine helped maintain his oxygen levels and prevent his health from deteriorating faster. It bought us time to scramble for an oxygen bed for further treatment. Without the concentrator, it would have been difficult to sustain for long," Simran tells The Better India. Like Girish, millions of COVID-19 patients across India are struggling to breathe during the initial stages of infection. Hospitals and the medical infrastructure are overwhelmed, resulting in a lack of oxygen beds and ventilators. If the administration of oxygen is delayed, a patient's health can deteriorate so fast that the results can be fatal. Aarti Nimkar, former president of the Indian Medical Association (IMA), Pune, says an oxygen concentrator can be a life-saver during cases in which a patient needs mild oxygen. "Ideally, oxygen levels in the body should be above 95. However, in COVID-19, the disease causes lung fibrosis and affects breathing among patients. A feeling of breathlessness, shortage of breath, chest pain and other respiratory issues are common symptoms. In such cases, the patients need oxygen therapy at the soonest, as the levels may start dropping. Such patients need assistance to compensate for inadequate breathing capabilities," she says, adding, "The device can help boost oxygen levels if they drop to 80-85." She adds that the devices are available in 5-10 litres per minute flow capacities, cost between Rs 25,000 and Rs 60,000, and should be used under the supervision of doctors. "The machine can buy crucial time for patients. They may rely on the device before the ambulance arrives and they are hospitalised," Aarti adds. Aarti says the device can help boost a patient's oxygen levels from 85 to up to 90 or 95, and even maintain these parameters to some extent. "Increased levels reduce the struggle for the patient and risks of health complications caused due to shortage of oxygen," she adds. Gujarat-based Ami Joshi, director of Ashmi Healthcare Private Limited says that over a hundred patients have benefited from oxygen concentrators since the surge in cases during the second wave. "The device is simple to use, as it does not have a manual regulator like oxygen tanks. It prevents excess discharge and can be handled by the patient as needed. The maintenance cost is low as it does not require refills. Only the water dehumidifier needs replacement as per the use. In some cases, two devices of 5 litres/per minute flow can be used for a single patient if required," she says. "The oxygen concentrator has also helped patients showing oxygen levels as low as 70," Ami says, adding that each machine is available on rent at Rs 400 or sometimes lent for free to people who cannot afford it. Explaining the functioning of the device Pune-based Sundeep Salvi, director of Chest Research Foundation (CRF), says, "The atmospheric air consists of about 21% oxygen, 78% nitrogen, and then other gases. The oxygen concentrator works by absorbing air from the surroundings and filtering out nitrogen and other gases. The oxygen is stored in a cylinder to be inhaled by the user." The machine operates on electricity and requires uninterrupted power supply with power-back ups. The machine starts releasing oxygen at the push of a button. The device filters nitrogen and increases the concentration of oxygen for inhalation. It is recommended to use the concentrator only if the SPO2 (oxygen saturation) level drops below 95. It is mandatory to have a doctor's approval to use the device. Use an oxygen mask or nasal cannula as recommended by the medical expert for inhalation. Ensure the filters are cleaned and do not block the air entry. It may affect the performance of the device. Patients with asthma, COPD and respiratory ailments can also use it if prescribed by the doctors. Sundeep cautions that an oxygen concentrator cannot be a replacement for oxygen or a ventilator. "It can only act as a cushion before the severity of the disease increases. Patients with moderate and severe health conditions will need higher doses of oxygen, and the device cannot meet those heavy requirements," he explains. "On many occasions, the severity increases dramatically. The oxygen levels in the patient drop suddenly. In such cases, the patient should be moved immediately to oxygen or ventilator beds. The oxygen concentrator will prove futile," he adds. Sundeep believes that oxygen concentrators can be more beneficial post-treatment. "The device can work as a support system during the recovery stage of the COVID-19, as here, smaller doses of oxygen are required. This way, bed occupancy at the hospital reduces, and the patient can continue the treatment at home. The vacated bed becomes available for another patient who is in more urgent need of oxygen or a ventilator," he adds. Sudha Khisti from Nagpur is one such COVID-19 patient recovering from the disease. "I was diagnosed on March 25 and remained hospitalised for almost 20 days. As I suffer from asthma, the doctor was concerned about my health and suggested I buy an oxygen concentrator," she says. The 68-year-old adds that moving out of the hospital reduced the chances of getting reinfected and her family members contracting COVID-19. "The device has proven to be a game-changer. After using it for a week, my oxygen levels have increased, and my dependency on the device has reduced. Earlier, I used it for almost five hours a day. But now, I use it only for a couple of hours. It has made me confident about my health," she says. Aarti emphasises that oxygen concentrators do benefit patients, especially in difficult situations. "It would be appreciated if the government can waive taxes or reduce the prices of these devices. It will make it more affordable for common people and prove beneficial in times of the pandemic," she adds. To procure an oxygen concentrator, please click here, here and here.

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An Introduction to oxygen therapyCocaine addiction is the compulsive use of cocaine despite adverse consequences. It arises through epigenetic modification (e.g., through HDAC, sirtuin, and G9a) and transcriptional regulation (primarily through FosB's AP-1 complex) of genes in the nucleus accumbens.Transcriptional and epigenetic mechanisms of oxygen therapyRole of HDAC inhibitors in cocaine addictionHistone deacetylase inhibitors (HDAC inhibitors) have been implicated as a potential treatment for cocaine addicts. HDACs are enzymes that can deacetylate the histones associated with genes. This can activate genes for transcription. Several experiments have shown that inhibiting HDACs involved in histone H3K9 deacetylation reduces drug seeking behavior.It has been known that epigenetic regulations, such as the methylation of H3K9, have a key role in the mechanism of addiction. Recent studies have shown that administering HDAC inhibitors can help reduce the craving for cocaine in rats. Trichostatin A (TsA) is an HDAC inhibitor associated with reduced cocaine-seeking behaviors; it inhibits HDAC classes 1, 3, 4, 6, and 10. Since this HDAC inhibitor has such a significant effect on cocaine-seeking behaviors, scientists have speculated about their ability to reduce a cocaine addict's risk of relapse in the rat model system during rehab.After several tests in which rats were exposed to cocaine followed by either an HDAC inhibitor or a placebo, it was found that HDAC inhibitors had a significant effect on lowering cocaine-seeking behavior. This also suggests an epigenetic mechanism involved in HDAC chromatin regulation. The data is crucial to proving the hypothesis that trichostatin A can remodel chromatin structure and prevent behavioral changes following cocaine exposure. Tests also revealed that HDAC inhibitor administration can not only prevent addiction, but also helps reduce the risk of a relapse in cocaine addicts in the rat model system.Role of HDAC5As the previous findings suggest, chronic cocaine use caused both alterations in the chromatin remodeling activity of HDACs and drug seeking behavior. Renthal et al. focused specifically on the class II histone deacetylase, HDAC5, since it was known to have activity-dependent regulation in neurons. In fact, they found that HDAC5 was a central regulator of the actions of chronic cocaine use and contributed to the behavioral adaptations with its deacetylase activity. Chronic cocaine injections increased HDAC5 phosphorylation at Ser259 in the nucleus accumbens (NAc) within 30 minutes. This provides docking sites for 14-3-3 proteins, which mediate the export of HDAC5 out of the nucleus. They also found that CaMKII was necessary for depolarization-induced HDAC5 phosphorylation in NAc tissue, highlighting its role as a kinase for HDAC5. Experiments with mutant proteins and HDAC inhibitors suggested that HDAC5's action is mediated through its catalytic histone deacetylase domain. Rapid phosphorylation and the export of HDAC5 from the nucleus following cocaine use most likely leads to increased pulses of acetylation, targeted gene activation, and behavioral adaptations to long-term cocaine exposure.The second set of experiments that Renthal et al. performed showed that chronic cocaine use induced upregulation of the NK1 receptor protein in HDAC5 knockout mice, which is associated with hyperacetylation of H3 at the NK1R gene promoter. The NK1R gene promoter has been associated with enhanced response to cocaine reward, meaning HDAC5 in normal genomes may decrease cocaine reward with chronic cocaine exposure. They also found key pathways that were implicated in neural plasticity and reward behavior, which included DA receptor signaling, ATF2/CREB signaling, NF-B, NFAT, cytoskeletal remodeling proteins, and ion channels. Their data implicated chromatin remodeling as a mechanism that drives altered gene activation and behavioral responses to cocaine. Using this they were able to conclude that within normal (wild type) genomes, the response to chronic cocaine includes phosphorylation of HDAC5 and export of the deacetylase out of the nucleus to activate downstream target genes. Between exposure and 24hours after, HDAC5 returns to the cell nucleus to limit expression of these cocaine regulated genes by histone deacetylation. Their experiments with HDAC5 knockout mice lent additional support for this hypothesis. Since HDAC5 isn't there to limit the gene's expression, it begins to accumulate with repeated cocaine exposure, with the end result being increased sensitivity to cocaine reward.Changes in critical H3K9me3 modificationsModifications to histones such as methylations and acetylations can change gene expression patterns by activating or deactivating a region of DNA for transcription. The H3K9 position has been shown by several studies to be altered by chronic cocaine use.Addictive behavior observed from long-term cocaine users can be due to changes of the gene expression profiles in the brain's reward circuitry. Most research has been focused on the active regions of the reward-related genes, but Maze et al. focuses at what happens to the heterochromatic regions. Maze et al. showed that heterochromatic regions in the nucleus accumbens (NAc), a major reward circuit in the brain, are significantly altered in the H3K9me3 position. Acute cocaine exposure leads to a rapid increase in H3K9me3 within half an hour and decreases back to normal levels within 24hours. Chronic cocaine exposure leads to a slower increase in H3K9me3 within an hour (although it reaches the same level as acute by this time) and a 50% decrease from normal baseline levels within 24hours. This chronic exposure was proposed to decrease heterochromatization (destabilization) within this brain region in patients given repeated cocaine exposure, which implies that the long-term addictive behaviors are affected by this epigenetic mark. They used ChIP-seq to provide supporting evidence that the H3K9me3 modification is mainly localized to intergenic regions. In these areas of the genome, 17 regions of repeat elements (SINEs, LINEs, LTRs, etc.) had significant H3K9me3 state changes in chronic cocaine exposure mouse models. They used quantitative PCR to determine that of these significant elements, the LINE-1 region showed a significant increase in expression levels. LINE-1 is a retrotransposon, so expressing it inappropriately can activate the transposon to insert itself within important genes and destabilizing the DNA. They conclude their findings by suggesting that LINE-1 retrotransposon insertions cause inappropriate or disrupted expression of genes leading to the addictive behavior.Treatment of oxygen therapyAs of May 2014update, there is no effective approved pharmacotherapy for cocaine addiction. HDAC inhibitors have been implicated as a potential treatment for cocaine addiction.Cognitive behavioral therapy is currently the most effective clinical treatment for psychostimulant addiction in general.
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