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The solution for both stomach pain and stomach ulcers is to kill parasites and bacteria quality serophene 100 mg menstruation japan, followed by dental and liver clean ups purchase serophene 50 mg line pregnancy urinary tract infection. You inhale it right along with the flies and roaches you may be trying to kill with arsenic-laced pesticides purchase 50 mg serophene with mastercard women's health questions online. Your nose and mouth mucous traps a lot of these whereupon you swallow them and they glide into the stomach buy cheap serophene 100 mg line women's health clinic lynchburg va. Your dentalware may be cleaned up in a few dental visits but the liver cleanses must go on for a year or two before it is reasonably clean. You may get pain relief in a few weeks but this should not derail your intention to revitalize yourself completely with a cleaned liver and stomach. Hiatal Hernia When bacteria have spread to the diaphragm and weak- ened it, along with the upper- stomach valve, food is al- lowed to get pushed up right through the diaphragm. The mother had platinum and tellurium in her milk (Salmonella can be transmitted in milk but this was not checked). It is quite possible the baby had these also, giving him a nasty tummy ache in addition to the gas pains. She was also chronically fatigued and had consumed enough antibiotic “to fill a room. We found Fasciolopsis, the intestinal fluke, in her stomach wall as well as in her intestine. She started the parasite program and in three weeks her appetite was back, in- somnia was gone, fatigue was better and a significant improvement was evident. Respiratory Illness Asthma is a very old disease described in the ancient literature. The only progress we have made to date with this disease is to give drugs to soothe the symptoms. One tries to cough them up, of course, but in our misguided effort to be polite we teach children to swallow anything they cough up! Some swallowing is inevitable and the young worms are back in the stomach, this time to set up their housekeeping in the intestine. Some never leave the stomach, causing children stomach aches and, of course, a large entourage of bacteria which, in turn, have their viruses. Most cases of Ascaris infestation also show Bacteroides fragilis bacteria which, in turn, carry the Coxsackie viruses (brain viruses). Whether or not these bacteria or viruses will thrive in you depends on whether you make a good home for them, namely have low immunity in some organ. The preferred organs for Bacteroides are liver and brain (brain tumors always show Bacteroides). The preferred organs for Coxsackie viruses appear to be tooth abscesses and brain. Not everybody with Ascaris develops asthma, even though they always go through a lung stage. That innocent cough of early childhood should not be ne- glected, as simply “croup. Kill their Ascaris with a zapper and keep it up daily or put parasite killing herbs in their food. Asthma sufferers become allergic to many air pollutants such as pollen, animal dander, smoke. The production of histamine in the lungs and the vast interconnectedness of histamine to allergies has been well studied scientifically. Then wash your hands and fingernails with grain alcohol, and let no more filth past your lips. For children wash hands before eating anything, even between meals; keep fingernails short. This could lead to massive infection, the kind that could result not only in asthma but seizures. Use cardboard, newspaper or anything that you can afford to throw away with the mess. If there is an asthmatic in your family, the whole family should be treated for Ascaris with a zapper or with the herbal parasiticides. Even after everybody including the pets have been treated, pets should not be allowed in the bedroom of the asth- matic person. It is also an al- lergic reaction, to the pet and to other inhaled bits of matter. Smoke of any kind, fragrance and chemicals of any kind, all household cleaners, polishes, and so forth should be removed. Install central air conditioning if possible, with maxi- mum filtering (but never with chemicals added to the filter and never with a fiberglass filter) at the furnace. The best place to recover is outdoors away from trees and bushes or indoors with total pollution-free air conditioning (free of asbestos, formaldehyde, arsenic, fiberglass, pet dander). When you suddenly need them, try to identify your source of reinfection or allergens. She was started on the herbal parasite program after killing Ascaris, Bacteroides and Coxsackie viruses with a frequency generator. She was immediately improved after cleaning up these sources and canceled her future appointment. Her lungs were full of benzalkonium (toothpaste), arsenic (ant poison under kitchen sink), zirconium (deodorant), and nickel from tooth metal. She had Ascaris and Naegleria, mycoplasma, Endolimax and the intestinal fluke in her lungs! She coughed up blood, after her doctor had diagnosed bronchiestasis recently, meaning her lungs were not capable of sweeping out the daily refuse we all breathe in. Going onto homeopathic medicine for stuffiness helped her avoid some hospital visits. It took several months (5 visits) to track her arsenic source to the bedroom car- pets (stain resistance! After steam cleaning it herself and doing a liver cleanse (after first killing parasites) she was amazed at her improvement. She had not been to the hospital in a month and was only using inhalers preventively. Her lungs had beryllium (coal oil) and asbestos, and two parasites, Paragonimus (lung fluke) and Ascaris. She got rid of the attacks but her cough and pneumonia bouts will continue until she moves from that house. Brett Wilsey, 70, was congested most of the time, had chronic sinus problems, was getting allergy shots for dust and mold, and was on several inhalers for his asthma plus emphysema. His blood test showed high “total carbon dioxide” or “carbonate” showing that his air exchange was not good.

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Opiates activate the chemoreceptor trigger zone in the medulla (by disinhibition) to cause nausea and vomiting serophene 100mg lowest price menopause underarm odor, and cough suppression also occurs because of the inhibitory effects of opiates on the brainstem nuclei in the cough reflex pathway buy 50mg serophene free shipping women's health clinic jensen beach fl. Dextro- methorphan is the non-opiate isomer of the opiate levorphanol and is an effective cough suppressant serophene 25mg line pregnancy ultrasound at 7 weeks. Sites in the monoamine nuclei such as the well-demonstrated actions of opioids on noradrenergic transmission in the locus coeruleus and enhancing dopamine-release in the ventral tegmental area (again via disinhibition) are likely to be associated with reward processes and so relate to dependence order 100 mg serophene visa menstruation occurs when there is a decrease in. Thus, although a patient prescribed morphine over a prolonged period of time will show signs of physical dependence, requiring slow reductions in dose at the end of treatment to avoid withdrawal, drug-seeking behaviour in these patients is very rare. However, with street use, psychological dependence on opioids is rapid to develop and overwhelming. The reason for this is unclear but it could result from the fact that pain is aversive, in that the stimulus produces not only a sensation of pain but also an unpleasant psychological effect. Perhaps this latter characteristic of pain switches off the reward systems in the cortex. The relative extent of the unwanted effects caused by selective agonists at the different opioid receptors is of great importance in determining if non-mu opioids will have better spectra of actions as compared to morphine. A lack of dependence is also seen with kappa agonists but is accompanied by aversive or non-rewarding effects that limit the usefulness of these agents in humans. Kelatorphan, an inhibitor of the peptidases which degrade the enkephalins, was thought be a novel route to analgesia by prolonging the duration of their actions. This protection of the enkephalins by the peptidase inhibitors has no dependence liability but as yet no peptidase inhibitor selective for the opioid peptides has been reported in humans. Opiates constrict the pupils by acting on the oculomotor nucleus and cause constipation by activating a maintained contraction of the smooth muscle of the gut which reduces motility. This diminished propulsion coupled with opiates reducing secretion in the gut underlie the anti-diarrhoeal effect. Although these effects are predominantly peripheral in origin there are central contributions as well. Morphine can also release histamine from mast cells and this can produce irritation and broncho- spasm in extreme cases. Opiates are used to relieve moderate to severe pain whatever the cause (accidents, post-operative pain, cancer, etc. Methadone: long duration and orally effective, thereby useful in weaning off heroin. Fentanyl: highly potent but with a short duration of action, used for short analgesia in surgical settings. Heroin (diacetylmorphine): a highly lipophilic drug but has very weak or no affinity for opiate receptors. It penetrates the brain rapidly whereupon it is metabolised to morphine which then binds to the mu receptor. Naloxone is a potent competitive antagonist at all three receptors with highest affinity for the mu receptor. It is used in cases of overdose, usually to reverse the respiratory depression but with the cost of also reversing the analgesia. However, it is very unclear that this has any bearing on their effects in patients, especially in cases where morphine effectiveness is reduced, such as in neuropathic pain. In terms of changes in opioid systems relevant to the control of pain after nerve injury, nerve damage can lead to a loss of opioid receptors such as the marked reduction in spinal opioid receptor number seen after nerve section. Although this may be an explanation of the poor effectiveness of opioids in post-amputation pains, less severe nerve damage, where opioids can also lack effectiveness, only slightly alters opioid receptor number. As discussed earlier, the changes that occur in the periphery and spinal cord after nerve damage can result in overexcitability of spinal neurons so that a hypersensitive state is induced. Quite simply, if neuronal excitability is dramatically increased then opioid controls may be insufficiently efficacious unless doses are increased sufficiently to increase the degree of inhibition required to balance the level of excitation. Here, the combination of a low dose of opioid, increasing inhibition, with a drug that blocks excitation such as ketamine may result in synergistic or additive effects that result in the desired degree of analgesia without adverse side-effects. Thus, this augmented opioid actions may counter the increased excitability without the need for large increase in doses of opioid. Alpha2 adrenoceptors appear to be important in this role but it is unlikely that behavioural effects such as sedation can be separated from the analgesia. This may be just one early step in the understanding of some of the chemistry of the psychological aspects of pain. Independently of their effects on mood, antidepressants increase activity in these descending control systems and are used as analgesics in neuropathic pain states. Individual differences in levels of pain, in the transition from acute to chronic pain, in susceptibility to neuropathic pain after nerve damage and in analgesic effectiveness may have a genetic basis. There is marked variability in animal genetic strains in terms of the sequelae of tissue and nerve damage and even in their responses to morphine. Given the huge range of human phenotypes, this may indicate important individual differences in susceptibility to pain and analgesia but we have no way of monitoring this possibility. It is therefore appropriate, but possibly foolhardy, to see if the two natural extremes of that excitability, namely sleep and waking, can be explained in terms of neurotransmitter activity. Of course, these states are not constant:our sleep can be deep or light and, even when we are awake, our attention and vigilance fluctuate, as the reading of these pages will no doubt demonstrate. Also, the fact that we sleep does not mean that our neurotransmitters are inactive:this would imply that sleep is a totally passive state, whereas all the evidence suggests that it is an actively induced process, subject to refined physiological control. In order to explain the physiological characteristics of the sleep±waking cycle, as well as how this might be controlled by different neurotransmitters and modified by drugs, we need to know which areas and pathways in the brain are vital to the induction and maintenance of this rhythmic behaviour. One is responsible for the basic circadian rhythm and ensures that our sleeping and waking periods normally occur at regular intervals. A second system fine-tunes this process and ultimately determines our precise functional status on the sleep±waking continuum. This is demonstrable not only in humans and laboratory animals, but also in invertebrates. Thus, while we cannot be sure that other animals sleep in the same way that we do, they do show a circadian cycle of motor activity. In some (nocturnal) species, such as the rat, this activity is actually highest during darkness. Even aplysia, the sea hare, has such a rhythm but this is more like that of humans in being maximally active during daylight (diurnal). Interestingly, when humans are in a time-free environment, the change in the rhythm of Neurotransmitters, Drugs and Brain Function. Generally, it becomes shorter (to as little as 20 h), rather than longer, which suggests that these cycles are regulated in different ways. Entrainment has also been shown in aplysia which, after exposure to a normal dark±light cycle, retains a cyclic pattern of activity for a number of days even if subjected to continuous light.

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Information travels from the soma cheap serophene 50 mg mastercard pregnancy journals week by week, along the axon 50mg serophene overnight delivery women's health clinic broadbeach, and to the terminal bouton buy serophene 25 mg line women's health clinic montreal, stimulating the Ca2+-mediated release of a neurotransmitter order 50mg serophene visa breast cancer jackets. Each neuron is also a functioning “bioelectric unit”, capable of generating and transmitting electrical information (sections 4. The ner- vous system is also rich in glial cells, which function as support cells. Glial cells are biosynthetically active cells possessing protein-laden membranes that offer a wealth of potential “druggable targets” for the medicinal chemist. There are four types of glial cells: astrocytes, oligodendrocytes, microglial cells and ependymal cells. Most importantly, they are neurochemically active and involved in the exchange of metabolites between neurons and the blood and also in the uptake of neuro- transmitter molecules from the synaptic cleft. Astrocytes are also an essential structural component of the blood–brain barrier (chapter 3), the most important pharmacokinetic hurdle to drug design for the central nervous system. Oligodendrocytes are responsible for producing and maintaining the myelin sheaths (fatty insulation layer) surrounding neu- ronal axons in the central nervous system. Not surprisingly, oligodendrocytes may play a role in multiple sclerosis (chapter 6). Microglia function as neural macrophages, respon- sible for phagocytosis (a defense mechanism which involves ingesting and removing par- ticles or substances foreign to the brain; from the Greek, phagein, to eat). In addition to providing druggable targets for the drug designer, glial cells are also important in medicinal chemistry because they are the primary source of brain tumors. This is not surprising, given the observation that glial cells are much more active in cellular division than neu- rons; brain cells, unlike other cells (e. Astrocytes are a frequent source of brain tumor, giving rise to astrocytomas and the extremely deadly glioblastoma multiforme. The development of anticancer agents for brain tumors is a technically challenging activity within medicinal chemistry. As a process, nerve conduction is vulnerable to (and use- ful for) a properly designed drug. A microelectrode placed into a cell will indicate a potential that is 50–80 mV more negative than the potential recorded by an electrode outside the cell. Inside the cell, there is a high K+ ion concentration (about 120 mM) and low Na+ concentration (about 20 mM); the reverse is true outside the cell. In addition, there is a negative charge inside the cell because the protein anions of the cytosol are not counterbalanced by cations. The difference between an ordinary cell and an excitable cell becomes evident when a depolarizing current is applied. In an ordinary cell, such as an erythrocyte, the trans- membrane potential is equal to zero; in a neuron, however, an explosive, self-limiting process allows the potential to overshoot zero and become about 30 mV more positive within the cell than outside it. This depolarization is called an action potential, and is carried first by sodium ions and then by potassium ions (see figure 4. The neuron is the fundamental anatomical unit of the brain; the action potential is the fundamental physiological (functional) unit of the brain. An action potential lasts only about a millisecond, during which time sodium rushes in and potassium rushes out through ion channel proteins opened by conformational change. The original ionic dis- equilibrium is then re-established through the rapid elimination of Na+ ions. In myelin- ated nerves, such ion exchange can occur only at the nodes of Ranvier, and the action potential jumps very rapidly from node to node without a loss of potential. This wave of depolarization passes along the axon to the nerve ending and can be repeated several hundred times per second. The action potential is the fundamental functional (physiological) unit of the brain and is the means of trans- mitting information within the nervous system. An action potential is generated by changes in the transmembrane voltage gradient across the neuronal membrane. The resulting wave of depolarization travels along the neuron as an electrical signal, transmitting information. Synaptic transmission is not electrical but chemical, and is triggered by the arrival of the action potential at the nerve ending. This causes a Ca2+ ion influx across the membrane and into the neuron, resulting in the release of an interneuronal chemi- cal messenger (neurotransmitter) characteristic for that particular neuron. There seem to be several different neurotransmitter release mechanisms, although none is well understood. When released, the neurotransmitter crosses the synaptic gap by passive diffusion and binds transiently to a receptor on the membrane of the postsynaptic neu- ron. The released neurotransmitter is then either destroyed enzymatically or taken back into the synapse and recycled. Inhibitory neurotransmitters, on the other hand, activate Cl− ion uptake through the postsynaptic neuronal membrane. This effect makes the intracellu- lar potential more negative than the original resting potential and thus hyperpolarizes the neuronal membrane. Naturally, a greater than normal impulse will be necessary to fire such a hyperpolarized neuron, since the threshold value of the action potential remains the same. Both excitatory and inhibitory impulses summate and trigger an all-or-none response of a particular neuron, on which hundreds of other neurons may synapse. Besides binding to postsynaptic receptors, a released neurotransmitter also “back- diffuses” to presynaptic receptors or autoreceptors on the neuron from which it was just released, fulfilling an important feedback regulatory function by facilitating or inhibit- ing transmitter release. It has been suggested that these presynaptic receptors are also heteroreceptors—that is, they respond to cotransmitters as well as neurotransmitters produced by the same neuron. For instance, it is known that neurotensin regulates the release of norepinephrine, its cotransmitter. Now that the fallacy of the “one neuron— one transmitter” dogma has been revealed, it is logical to assume that multiple trans- mitters (neurotransmitter plus a cotransmitter) may regulate each other’s release and metabolism in a given synapse and that there may be considerable overlap among presynaptic auto- and heteroreceptor functions. To be defined as a classical neuro- transmitter, a molecule must be synthesized and stored in a neuron, released from that neuron in a Ca2+ dependent process, diffuse to an adjacent neuron, specifically dock with a receptor on that adjacent neuron, and have its binding to this receptor blocked by a competitive antagonist. A neuromodulator, on the other hand, is a molecule which is present in the synaptic cleft and which modifies either the frequency or the efficiency of the neurotransmitter molecule, thereby either amplifying or attenuating the neuro- transmitter action. The traditional neurotransmitters have been recognized for a number of decades and include acetylcholine, norepinephrine, and glutamate. At this point it is well to consider that the classical definitions and concepts in this field have been undergoing considerable change, and that the distinctions between neurotransmitters, cotransmitters, neuromodulators, and neurohormones often become blurred. Many peptide hormones of the hypothalamus and hypophysis, for instance, have been recognized as having neurotransmitter activity at other sites, and neurohormones and the discipline of neuroendocrinology have become increasingly important in the biosciences. In recent decades, an explosive development in the discovery of cotransmitters has greatly expanded our understanding of neurotransmission, and of the homeostatic equi- librium that is regulated by aminergic and peptidergic cotransmitters even in systems as simple as that of Hydra. Postsynaptically, cotransmitters can influence the same recep- tor on the target, bind to two different receptors on the same target, or bind to two dif- ferent receptors on two different targets.

Additional information Common and Immediate:Pyrexialreactions trusted serophene 100 mg women's health center tualatin,anaphylaxisand urticariahave beenreportedrarely order serophene 25 mg visa pregnancy halloween shirts. Significant * Levofolinate may #levels or effect of the following drugs: interactions possible #efficacy of folic acid antagonists cheap serophene 100mg line pregnancy lingerie, e serophene 100 mg overnight delivery menopause kits boots. This assessment is based on the full range of preparation and administration options described in the monograph. Pre-treatment checks * Avoid in severe heart failure, second- and third-degree heart block and sinus node dysfunction (unless a pacemaker is fitted) and cardiogenic shock. Inspect visually for particulate matter or discolor- ation prior to administration and discard if present. Inspect visually for particulate matter or discolor- ation prior to administration and discard if present. Disopyramide | 267 Technical information Incompatible with No information Compatible with Flush: NaCl 0. This is more likely in patients with cardiomyopathy or uncompensated congestive heart failure. Additional information Common and serious Anticholinergic effects such as dysuria, acute urinary retention (more undesirable effects likely in patients with prostatic enlargement), disorders of accommodation, diplopia, dry mouth. This assessment is based on the full range of preparation and administration options described in the monograph. Its use requires intensive haemodynamic monitoring and ideally should be confined to the critical care setting. Dobutamine | 269 * It may also be used in cardiac stress testing if the patient cannot undergo a period of exercise or if the exercise yields no useful information (dobutamine stress echocardiography). Pre-treatment checks * Do not use in mechanical obstruction of ventricular filling and/or outflow, hypovolaemia. Biochemical and other tests (not all are necessary in an emergency situation) Bodyweight Electrolytes: serum K Dose Inotropic effect: initiate at 2. Cardiac stress testing: initially 5 micrograms/kg/minute for 3--8 minutes increasing by 5 micrograms/kg/minute every 3--8 minutes, up to a usual maximum of 20 micrograms/kg/minute (occasionally up to 40 micrograms/kg/minute may be required). Continuous intravenous infusion via a syringe pump The concentration used is dependent on the patient’s dosage and fluid requirements but the final concentration must be no greater than 5mg/mL. Withdraw 250mg (20mL) of the concentrate and make up to 50mL in a syringe pump with Gluc 5% or NaCl 0. Cap the syringe and mix well to give a solution containing 5mg/mL (5000 micrograms/mL). Inspect visually for particulate matter or discoloration prior to administration and discard if present. Calculation of infusion rate: Weight ðkgÞÂrequired rate ðmicrograms=minuteÞÂ60 Infusion rate ðmL=hourÞ¼ Concentration of prepared infusion ðmicrograms=mLÞ See Table D6 below for a dosage chart detailing pre-calculated infusion rates for each bodyweight using a 5mg/mL (5000 micrograms/mL) solution. Aciclovir, alteplase, aminophylline, amphotericin, bumetanide, calcium gluconate, ceftazidime, digoxin, doxapram, drotrecogin alfa, flucloxacillin, foscarnet, furosemide, heparin sodium, insulin (soluble), micafungin, midazolam, pantoprazole, phenytoin sodium, phytomenadione, piperacillin with tazobactam. Stability after From a microbiological point of view, should be used immediately; however, preparation prepared infusions may be stored at 2--8 C and infused (at room temperature) within 24 hours. Blood glucose At least 12-hourly * May see "insulin requirements in patients with diabetes mellitus. Response to therapy After 72 hours * Tolerance may develop after 72 hours of therapy. Other: headache, bronchoconstriction, eosinophilia, #platelet aggregation with prolonged therapy, nausea, urinary urgency. This assessment is based on the full range of preparation and administration options described in the monograph. T able D obutam in e rate ofin fusion usin g dobutam in e 2 m g m ade up to5 m L in a 5 - m L syrin ge pum p ( 5 m icrogram s/ m L I nfusi onrate ( m i crog ram s/ kg / i nute) 1 W ei g h t R ate ofi nfusi on( m h our) i nkg 4 4 5 5 6 6 7 7 8 8 9 9 1 1 1 1 1 Dopamine hydrochloride | 273 Dopam ine hydrochloride 40mg/mL and 160mg/mL solution in 5-mL ampoules 40mg/mL solution in 5-mL and 10-mL vials 400mg (1. Its use requires intensive haemodynamic monitoring and ideally should be confined to the critical care setting. Pre-treatment checks * Do not use in phaeochromocytoma, hyperthyroidism, uncorrected atrial or ventricular tachy- arrhythmias, ventricular fibrillation. Continuous intravenous infusion The concentration used is dependent on the patient’s dosage and fluid requirements. The solution should be clear and almost colourless (the concentrate may have a pale straw colour). Inspect visually for particulate matter or discoloration prior to administration and discard if present. Continuous intravenous infusion via a syringe pump For administration via a central line only. Withdraw 200mg of the concentrate and make up to 50mL in a syringe pump with NaCl 0. Cap the syringe and mix well to give a solution containing 4mg/mL (4000 micrograms/mL). The solution should be clear and almost colourless (the concentrate may have a pale straw- colour). Inspect visually for particulate matter or discoloration prior to administration and discard if present. Calculation of infusion rate: Weight ðkgÞÂrequired rate ðmicrograms=minuteÞÂ60 Infusion rate ðmL=hourÞ¼ Concentration of prepared infusion ðmicrograms=mLÞ See Tables D8, D9 and D10 below for dosage charts detailing pre-calculated infusion rates for each bodyweight using 1. Dopamine hydrochloride | 275 Technical information Incompatible with Sodium bicarbonate. Aciclovir, amphotericin, ampicillin, alteplase, benzylpenicillin (penicillin G), furosemide, gentamicin, insulin (soluble). Stability after From a microbiological point of view, should be used immediately; however, preparation prepared infusions may be stored at 2--8 C and infused (at room temperature) within 24 hours. Monitoring Measure Frequency Rationale Blood pressure Continuously * Response to therapy. Infusion site * Possible necrosis on extravasation; see Additional information below for management. Benefits of continued dopamine infusion should be weighed against the risk of possible necrosis. Renal function Periodically * Monitor particularly during high dose regimens (>20 and serum Na microgram/kg/minute) as decreased renal blood flow can and K occur. Additional information Common and serious Infusion-related: Local: Extravasation -- necrosis and sloughing of the undesirable effects surroundingtissue. Ischaemiacanbe reversedbyinfiltrationofthe affectedarea with phentolamine (see the Phentolamine monograph). This assessment is based on the full range of preparation and administration options described in the monograph. Dopamine hydrochloride | 277 Table D8 Dopamine rate of infusion using dopamine 400 mg in a 250-mL infusion bag, i. It stimulates beta -adrenoceptors and2 peripheral dopamine receptors; it inhibits neuronal uptake of noradrenaline. Pre-treatment checks * An inadequate circulating blood volume should be restored prior to and during treatment with dopexamine. This can be increased to 1microgram/kg/minute and further increased up to 6micrograms/kg/minute in increments of 0.

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