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Avana

By C. Kirk. Seattle University. 2019.

Development of Throughout treatment * Development of severe avana 100 mg, persistent diarrhoea may diarrhoea be suggestive of Clostridium difficile-associated diarrhoea and colitis (pseudomembranous colitis) 200mg avana. Additional information Common and serious Immediate: Anaphylaxis and other hypersensitivity reactions have been undesirable effects reported 200 mg avana. Other: Nausea 100 mg avana, vomiting 100mg avana, diarrhoea avana 200 mg, taste disturbances avana 50 mg, tooth or tongue discoloration avana 100mg, hearing loss 50mg avana, blood disorders 50 mg avana, positive Coombs’ test, rash, pruritus,urticaria,Stevens--Johnsonsyndrome,rarelytoxicepidermalnecrolysis, exfoliative dermatitis, myoclonic activity, convulsions, confusion, mental disturbances. This assessment is based on the full range of preparation and administration options described in the monograph. Inflixim ab 100-mg dry powder vial Infliximab should be used under specialist supervision only. Pre-treatment checks * Screen for tuberculosis, do not give to patients with active tuberculosis or other severe infections. If the condition has responded, maintenance of either 5mg/kg 6 weeks after initial dose, then 5mg/kg every 8 weeks or a further dose of 5mg/kg if signs and symptoms recur. If the condition has responded, consult product literature for guidance on further doses. If there is no response at 6 weeks, no additional treatment with infliximab should be given. If there is no response after 14 weeks, no additional treatment with infliximab should be given. Confirm the patient’s details on the prepared bag, and that the correct dose has been supplied. Inspect visually for particulate matter or discoloration prior to administration and discard if present. Technical information Incompatible with No information Compatible with Flush: NaCl 0. However, prepared infusions are known to be stable if stored at 2--8 C and infused (at room temperature) within 24 hours. Monitoring Measure Frequency Rationale Close observation For 1--2 hours post * Most hypersensitivity reactions are reported for hypersensitivity infusion during this period. Additional information Common and serious Immediate (or with a few hours of administration): Anaphylaxis and other undesirable effects hypersensitivity reactions have been reported. Other: Viral infection, serum sickness-like reaction, headache, vertigo, dizziness, flushing, lower and upper respiratory tract infection, abdominal pain, diarrhoea, nausea, dyspepsia, "transaminases, urticaria, rash, pruritus, hyperhidrosis, dry skin, chest pain, fatigue, fever, blood dyscrasias. This assessment is based on the full range of preparation and administration options described in the monograph. Insulins Insulin 100 units/mL solution in 10-mL vials 3-mL pen cartridges and 3-mL pre-filled pens (see chart below) Restricted use: insulin 500 units/mL solution in 10-mL vials * Insulin is a hormone produced by the pancreas that is crucial in the regulation of carbohydrate, protein and fat metabolism. It is secreted when blood glucose levels start to rise; its action is opposed byglucagon; catecholamines,glucocorticoidsand growth hormone (thecounter-regulatory hormones), and others. Decreased or absent insulin secretion results in the development of diabetes mellitus, although patients with insulin resistance may be markedly hyperinsulinaemic as well as hyperglycaemic. If used it must be kept completely separate from all other insulins, be clearly labelled, and only be administered by staff who have had specific training in its use. Insulin is used in combination with aggressive rehydration, potassium supplementation and many other supportive measures, alongside intensive monitoring. Insulin is used in combination with rehydration, potassium and other supportive measures, alongside intensive monitoring. Once the patient is biochemically stable and able to eat/drink, the usual therapy for diabetes treatment should be resumed or started. Moderate to severe hyperkalaemia (unlicensed): calcium gluconate is given to stabilise the myocardium (see Calcium gluconate monograph) followed by 5--10 units of soluble insulin with Insulins | 453 50mL Gluc 50% over 5--15 minutes. Maintenanceregimens forinsulin-dependentorinsulin-requiringdiabetesmellitus: the regimen chosen depends on the patient’s ability to inject, monitor and adjust doses, patient prefer- enceandthedegree of blood glucosecontrolrequired. Occasionally abiphasic insulin is used, but the dose must then be given in association with a meal. Dose in renal impairment: reduced doses may be required in severe renal impairment. Check that the insulin you have selected is the one specified on the prescription chart. If using an insulin suspension, re-suspend by rolling the vial, cartridge or pen gently between the palms or inverting several times. Withdraw the required dose using an insulin syringe*, or dial up the correct dose according to the manufacturer’s instructions if using an insulin pen. Using an area on the abdomen, outer thigh, upper outer arm or the buttock, pinch up a skin fold between the thumb and forefinger and hold throughout the injection. Avoid overuse of injection sites as this may impair absorption; rotate sites so that individual sites are not reused within 1 month. Continuous intravenous infusion via a syringe pump This method is used for control of blood glucose. 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. In use: May be used and stored at room temperature for up to 28 days (some products are stable for 42 days -- see individual product literature). Pens in use should not be stored in the fridge (pens may jam) or with needles attached. Monitoring of Annually (or more frequently * To ensure that complications are treated or diabetic if appropriate) dealt with, and that the patient is counselled complications appropriately. Additional information Common and Injection/infusion-related: serious * Too rapid administration: Hypoglycaemia. Lipoatrophy or lipohypertrophy from overuse of sites (less common with highly purified insulins). Action in case of Symptoms to watch for: Hypoglycaemia: excessive sweating, pallor, palpitations, overdose trembling, feeling cold, impaired vision, irritability, tingling round the lips, inability to concentrate, confusion, personality change, inability to waken. Counselling Correct administration of insulin, insulin storage, disposal of sharps, importance of taking doses regularly as prescribed. Training in use of blood glucose, blood ketone or urine glucose monitoring as appropriate. Patients maintained on insulin should always carry glucose (and glucagon if necessary) and should be able to recognise the symptoms of hypoglycaemia. Relatives or carers should be trained to recognise hypoglycaemia and how to treat it appropriately. This assessment is based on the full range of preparation and administration options described in the monograph. Intralipid 10% emulsion in 100-mL and 500-mL infusion containers 20% emulsion in 100-mL, 250-mL and 500-mL infusion containers 30% in 333-mL infusion container * Intralipid contains fractionated soya oil in the form of a fat emulsion. It is a rich source of linoleic and linolenic acids, which are essential fatty acids. Energy requirements of individuals must be metif aminoacidsaretobeutilisedfor tissuemaintenanceratherthan asanenergy source. Parenteral feeding should be introduced slowly initially, particularly in those patients at risk of refeeding syndrome, e. Treatment of local anaesthetic induced cardiac arrest that is unresponsive to standard therapy: data is still extremely limited; there are no standard methods for lipid emulsion therapy. Intravenous infusion * Intralipidmay be given as a separate infusion or (more commonly now) as an ‘all-in-one’ admixture. Subsequently the dose is usually increased and, when a larger intake is indicated, the dose may be increased to a maximum of 3g/kg/day. Fat emulsions may extract phthalate plasticisers from bags and giving sets and non-phthalate containing equipment should be used wherever possible. Compatible with Solutions: May be added to certain amino acid and carbohydrate solutions. Monitoring Measure Frequency Rationale Fat elimination and Throughout treatment * Patients with conditions involving impaired lipid triglycerides (daily in high-risk metabolism are at risk of fat embolism. Vitamins and trace * Deficiency can occur, especially in patients elements receiving long-term parenteral nutrition. Additional information Common and serious Immediate: Anaphylaxis and other hypersensitivity reactions have very rarely undesirable effects been reported. Infusion-related: Too rapid administration: Prolonged or too rapid infusion of soya oil emulsion or its use in patients with impaired fat metabolism has been associated with the ‘fat overload syndrome’: hyperlipidaemia, fever, fat infiltration, organ dysfunction and coma. Significant * Intralipid may #levels or effect of the following drugs: interactions coumarin anticoagulants (soybean oil has natural vitamin K1 content). This assessment is based on the full range of preparation and administration options described in the monograph. Patient Safety Alert: Safer Practice with Epidural Injections and Infusions March 2007. Iron dextran (Cosm oFer) Iron (as iron dextran) 50mg/mL solution in 2-mL, 5-mL and 10-mL ampoules * Iron isan essential element, being necessaryfor haemoglobin formation and thestorage of oxygen in living cells. Pre-treatment checks * Not to be given in: history of allergic disorders including asthma and eczema; infection; active rheumatoid arthritis; severe hepatic impairment; acute renal failure. Formoderatelyactivepatients,give injections daily into alternate buttocks; in relatively inactive or frail patients, give injections once or twice weekly. If the calculated total dose required exceeds 20mg/kg/ day, the administration must be split over two days (see Table I6 below). Dose calculation for iron-deficiency anaemia: the desired dose may be calculated from the following equations (dependent on theunit of measure for Hb), which apply to abodyweight >35kg; or use Table I6 below. For Hb reported in g/dL: Total dose required ðmg ironÞ¼½bodyweight ðkgÞÂðtarget HbÀactual HbÞÂ2:4Šþ500 For Hb reported in mmol/L: Total dose required ðmg ironÞ¼½bodyweight ðkgÞÂðtarget HbÀactual HbÞÂ3:84Šþ500 Iron replacement for blood loss: the aim is to replace the iron content of the estimated blood loss. Intermittent intravenous infusion (preferred route) Preparation and administration 1. Inspect visually for particulate matter or discoloration prior to administration and discard if present. Observe the patient carefully for signs of allergic reac- tion for at least 60 minutes; if no adverse effects are seen give the remainder of the dose. Withdraw the required dose (or the remainder of the dose if a test dose has been given). Up to 2mL may be given at each administration (total dose required is determined by dosage calculation). Attach a 20--21GÂ50-mm needle for average-sized adults (use 23GÂ32-mm needle for smaller adults; 20--21GÂ80--100-mm needle for obese adults). The patient should be positioned in the lateral position with the injection site uppermost, or standing bearing their weight on the leg opposite the injection site. Leave the needle in situ for a few seconds before withdrawal to allow the muscle mass to accom- modate the injection volume. To minimise leakage up the injection track, the patient should be advised not to rub the injection site. Intravenous injection (or injection into the venous limb of a dialyser) Preparation and administration 1. Withdraw the required dose (2--4mL) and dilute to a final volume of 10--20mL with NaCl 0. Inspect visually for particulate matter or discoloration prior to administration and discard if present. Observe the patient carefully for signs of allergic reaction for at least 15 minutes; if no adverse effects are seen, give the remainder of the injection. Technical information Incompatible with No information Compatible with Flush: NaCl 0. 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 Hypersensitivity or Throughout * Discontinue therapy immediately if this occurs. Respiratory Throughout * Respiratory difficulties such as dyspnoea have observations administration been reported -- discontinue treatment if they occur. Total iron-binding Periodically * Useful to assess saturation of the system when the capacity treatment cycle completed, to decide whether response has been satisfactory, and also to assess iron overload. Additional information Common and serious Immediate: Anaphylactoid and other hypersensitivity reactions have been undesirable effects reported. Other: "risk of allergic reactions in patients with immune or inflammatory conditions (e. Symptoms include arthralgia, myalgia, pyrexia, urticaria, rashes, itching, nausea, shivering (rarely respiratory difficulty, angioedema and cardiovascular collapse); cramps; blurred vision. Chronic repeated administration of iron at high doses can cause liver accumulation, leading to fibrosis as a result of inflammation. Pharmacokinetics Elimination half-life is 5 hours for circulating iron; 20 hours for total iron (bound and circulating). Significant * Iron dextran may "levels or effect (or "side-effects) of dimercaprol (avoid interactions combination -- may result in serious toxicity). This assessment is based on the full range of preparation and administration options described in the monograph. Iron sucrose (Venofer) 20mg/mL solution in 5-mL ampoules * Iron isan essential element, being necessaryfor haemoglobin formation and thestorage of oxygen in living cells. Shouldtreatmentwithironsucrosebecontemplatedinthesepatients,afulltreatment plan (including monitoring and treatment of hypersensitivity reactions) should be prepared. Pre-treatment checks * Not to be given in: history of allergic disorders including asthma and eczema.

This assessment is based on the full range of preparation and administration options described in the monograph avana 200mg. Pre-treatment checks * Avoid in acute bacterial endocarditis avana 200 mg, major bleeding or high risk of uncontrolled haemorrhage including recent haemorrhagic stroke avana 100 mg. If treatment is required beyond 8 days avana 50 mg, reduce the dose to either 5000 units (women <80kg avana 100mg, men <70kg) or 7500 units (women! For treatment doses either monitor anti-Factor Xa levels or use unfractionated heparin 100mg avana. For treatment doses either monitor anti-Factor Xa levels or use unfractionated heparin 100 mg avana. Dose in hepatic impairment: the manufacturer advises to avoid in severe hepatic impairment avana 50mg. Pinch up a skin fold on the abdominal wall between the thumb and forefinger and hold through- out the injection 50mg avana. Dalteparin sodium | 199 Intravenous infusion via a syringe pump (haemodialysis only) Preparation and administration 1 200 mg avana. Technical information Incompatible with No information Compatible with Flush: NaCl 0. In use: Vials should be stored below 30 C and contents used within 14 days of first use. Stability after From a microbiological point of view, prepared infusions should be used preparation immediately; however, the preparation is known to be stable at room temperature for up to 24 hours. Monitoring Measure Frequency Rationale Platelets Alternate days from * Thrombocytopenia can occur in this period of therapy. Serum K After 7 days * Heparins #secretion of aldosterone and so may cause "K (especially in chronic kidney disease). Bleeding Throughout treatment * Low bodyweight: In women <45kg and men <57kg there is a higher risk of bleeding with prophylactic dalteparin doses. Anti-Xa activity If indicated * Not required routinely but may be considered in patients at "risk of bleeding or actively bleeding. Other: Risk of bleeding with organic lesions, invasive procedures, asymptomatic thrombocytopenia during the first days of therapy, clinically significant "K in patients with diabetes or chronic renal failure. This assessment is based on the full range of preparation and administration options described in the monograph. Danaparoid should be started preoperatively; thelast preoperative dose being given a minimum of 1--4 hours before surgery. Pinch up a skin fold on the abdominal wall between the thumb and forefinger and hold through- out the injection. Inspect visually for particulate matter or discolor- ation prior to administration and discard if present. Intravenous infusion via a syringe pump Preparation of a 200 anti-Factor Xa units/mL infusion with a total volume of 22. Inspect visually for particulate matter or discolor- ation prior to administration and discard if present. Technical information Incompatible with No information Compatible with Flush: NaCl 0. Monitoring Measure Frequency Rationale Platelet count (patients Daily * To rule out cross-reactivity (#platelets). Signs and symptoms Continuously * If danaparoid is administered in the context of of neurologic peridural or spinal anaesthesia, extreme vigilance impairment (peridural and frequent monitoring must be exercised to or spinal anaesthesia) detect any signs and symptoms of neurologic impairment, such as back pain, sensory and motor deficits (numbness and weakness in lower limbs) and bowel or bladder dysfunction. The risk is increased by the prolonged use of these routes, by the concomitant use of drugs affecting haemostasis, e. Protamine sulfate only partially neutralises overdose the anticoagulant effect of danaparoid and cannot be relied on to reverse bleeding associated with overdosage. This assessment is based on the full range of preparation and administration options described in the monograph. Dantrolene sodium 20-mg dry powder vials * Dantrolene sodium is a muscle relaxant acting directly on skeletal muscle, thus reducing muscle contractility in response to excitation. Pre-treatment checks As soon as the malignant hyperthermia syndrome is recognised, stop all anaesthetic agents. The manufacturers note that a 70-kg man may require approximately 36 vials (to give 10mg/kg) and that such a volume could be administered in approximately 11/2 hours. Further doses are given during anaesthesia if signs of malignant hyperthermia develop. Dantrolene sodium | 205 Intravenous injection Preparation and administration Dantrolene sodium is incompatible with NaCl 0. Inspect visually for particulate matter or discoloration prior to administration and discard if present. Intermittent intravenous infusion Preparation and administration Dantrolene sodium is incompatible with NaCl 0. Inspect visually for particulate matter or discoloration prior to administration and discard if present. Technical information Incompatible with Dantrolene sodium is incompatible with NaCl 0. The powder may have a mottled orange/white appearance or be in the form of loose aggregates; this does not affect the stability of the product. Displacement value Negligible Stability after preparation From a microbiological point of view, should be used immediately; however, reconstituted vials may be stored at 15--30 C for 6 hours. Additional information Common and serious Infusion-related: undesirable effects * Too rapid administration: Side-effects tend to occur at the start of treatment but are often short lived and can be controlled by adjusting the dose. Rarely diarrhoea may develop and be severe enough to require cessation of treatment. If diarrhoea recurs on restarting dantrolene then the treatment should be stopped permanently. Significant * Dantrolene may "levels or effect of the following drugs (or "side-effects): interactions calcium channel blockers ("risk cardiovascular depression and "K), vecuronium ("neuromuscular block). This assessment is based on the full range of preparation and administration options described in the monograph. Daptom ycin 350-mg, 500-mg dry powder vials * Daptomycin is a cyclic lipopeptide antibacterial. Dose in renal impairment: adjusted according to creatinine clearance:1 * CrCl 30--50mL/minute: dose as in normal renal function. Dose in hepatic impairment: no dose adjustment necessary in mild to moderate impairment (Child--Pugh Class A or B) but insufficient experience is available with Child--Pugh Class C, therefore caution should be exercised. Intermittent intravenous infusion Preparation and administration Daptomycin is incompatible with Gluc solutions. Gently swirl the vial (do not shake) for a few minutes until a clear solution has developed. Inspect visually for particulate matter or discoloration prior to administration and discard if present. Withdraw the required dose by slowly pulling the syringe plunger all the way to end of the syringe to remove the entire vial contents. Expel air, large bubbles and any excess solution to obtain the required dose and add to a suitable volume of NaCl 0. Intravenous injection Preparation and administration Daptomycin is incompatible with Gluc solutions. Gently swirl the vial (do not shake) for a few minutes until a clear solution has developed. Inspect visually for particulate matter or discoloration prior to administration and discard if present. Withdraw the required dose by slowly pulling the syringe plunger all the way to end of the syringe to remove the entire vial contents. Technical information Incompatible with Daptomycin is incompatible with Gluc solutions. Displacement value Negligible Stability after From a microbiological point of view, should be used immediately, however: preparation * Reconstituted vials may be stored at 2--8 C for 24 hours. Renal function Periodically * If renal function changes a dose adjustment may be necessary. Development of Throughout and up to * Development of severe, persistent diarrhoea may be diarrhoea 2 months after suggestive ofClostridiumdifficile-associated diarrhoea treatment and colitis (pseudomembranous colitis). Additional information Common and serious Immediate: Anaphylaxis and other hypersensitivity reactions have rarely been undesirable effects reported. Other: Fungal infections, headache, nausea, vomiting, diarrhoea, rash, "pulse, metallic taste. Pharmacokinetics Elimination half-life is 7--11 hours (>27 hours if CrCl <30mL/minute). Significant * "Risk of myopathy with the following (preferably avoid combination): interactions ciclosporin, fibrates, statins. Action in case of Antidote: No known antidote, but haemodialysis or peritoneal dialysis may overdose clear daptomycin slowly. This assessment is based on the full range of preparation and administration options described in the monograph. When given by injection it forms a stable water-soluble iron-complex (ferrioxamine) that can be excreted in the urine and in bile. However, it may exacerbate aluminium-related encephalopathy and precipitate seizures. Pre-treatment checks * Not recommended for use in pregnancy or lactation, and has been found to be teratogenic in animal studies (especially in the first trimester). The risks and benefits of treatment should be assessed before considering chelation therapy in pregnancy or lactation. Baseline ophthalmic assessment (visual field Serum aluminium level (in diagnosis and treat- measurements, funduscopy, colour vision test- ment of aluminium overload in end-stage renal ing using pseudoisochromatic plates and the failure). Farnsworth D-15 colour test, slit lamp investiga- Serum ferritin (in chronic iron overload). Serum iron taken at about 4 hours after ingestion Baseline U&Es (may require dose adjustment in is the best laboratory measure of severity of renal impairment; treatment of aluminium over- overdose: load may result in #Ca). Diagnosis of aluminium overload in end-stage renal failure: recommended in patients with serum aluminium levels >60 nanograms/mL associated with serum ferritin levels >100 nanograms/ mL. An increase in serum alumin- ium above baseline of >150 nanograms/mL is suggestive of aluminium overload; a negative test does not eliminate the possibility of aluminium overload. Treatment of aluminium overload in end-stage renal failure: indicated if the patient is symptomatic owing to organ impairment, or if aluminium level is consistently >60 nanograms/ mL associated with a positive desferrioxamine test (see above). Dose in renal impairment: dose as in normal renal function but elimination of chelated metals may be impaired in severe renal impairment -- haemodialysis is advised. Inspect visually for particulate matter or discolor- ation prior to administration and discard if present. It may be possible to further "iron excretion by infusing the same daily dose over a 24-hour period. Inspect visually for particulate matter or discolor- ation prior to administration and discard if present. Technical information Incompatible with Heparin sodium Compatible with Flush: NaCl 0. Displacement value Negligible Stability after From a microbiological point of view, should be used immediately; however: preparation * Reconstituted vials may be stored below 25 C for 24 hours (do not refrigerate). Monitoring Measure Frequency Rationale U&Es At least every 3 months * Caution in renal impairment as metal during therapy complexes areeliminatedrenally. Ifclinicallyindicatedfollowingrisk-- benefit assessment, treatment can be restarted at lower doses with intensive ophthalmic review throughout treatment. Audiological review * Disturbances in hearing reported, especially when using high doses of desferrioxamine or in patients with low ferritin levels. Ifclinicallyindicatedfollowingrisk-- benefit assessment, treatment can be restarted at lower doses with intensive audiological review throughout treatment. Urinary iron excretion Regularlythroughtherapy * To assess degree of iron chelation in order to tailor dose regimen. Respiratory function Ongoing during therapy * Pulmonary complications, including fatal acute respiratory distress syndrome, have been reported in cases of long-term or high- dose therapy. Cardiac function As clinically indicated * When desferrioxamine used in conjunction with ascorbic acid (vitamin C) -- see significant drug interactions below. Additional information Common and serious Immediate: Anaphylaxis and angioedema have very rarely been reported. Significant * The following may "desferrioxamine levels or effect (or "side-effects): interactions ascorbic acid(oral dosesofup to 200mg dailymay "iron complex excretion -- which may impair cardiac function. Compliance is a major issue with long-term treatment -- invest time in counselling and planning to facilitate concordance and compliance. This assessment is based on the full range of preparation and administration options described in the monograph. In its injectable form it is used: * To diagnose cranial diabetes insipidus; assess renal concentration capacity; to test for fibrino- lytic response. Diagnostic testing * When used for diagnostic purposes, fluid intake must be limited to that required to satisfy thirst, and must not exceed 500mL from 1 hour before until 8 hours after administration. Biochemical and other tests Bodyweight (in some indications) Baseline plasma osmolarity or baseline body- Baseline blood pressure and pulse weight (to enable monitoring of fluid balance) Electrolytes: Serum Na, K Dose Forexistingdiabetesinsipiduspatientsswitchedfrommaintenancetoparenteraldosing: * Intranasal 10 micrograms ffi parenteral 1 microgram. Failure to produce concentrated urine after water deprivation, followed by the ability to do so after the administration of desmopressin, confirms a diagnosis of cranial diabetes insipidus. Failure to concentrate after the administration suggests nephrogenic diabetes insipidus. In patients with a normal response the sample should show fibrinolytic activity of euglobulin clot precipitate on fibrin plates of! For surgical patients, unless contraindicated, give tranexamic acid orally from 24 hours beforehand until healing is complete. Alternatively, 4 micrograms can be given prophylactically immediately prior to lumbar puncture and 24 hours later. Inspect visually for particulate matter or discolor- ation prior to administration and discard if present.

100 mg avana

The lungs of premature infants often fail to produce adequate amounts of surfactants required for breathing 50mg avana. This life threatening condition called Infant Respiratory Distress Syndrome can now be treated with artificial lung surfac- tants developed in the 1980s avana 100mg. When introduced into the lungs of the infant these surfactants often stabilize breathing till the alveoli begin to produce sur- factants on their own 200mg avana. Cold-blooded animals such as frogs avana 200 mg, snakes and lizards do not need lung surfactants for breathing avana 100 mg. As a result they require about a factor of ten less oxygen than warm- blooded animals of comparable size 100 mg avana. Therefore avana 50 mg, cold-blooded animals can function with correspondingly smaller lung surface area 100mg avana. The alveolal radii of these animals are ten times larger than those of warm-blooded animals (see Exercise 9-9) avana 50mg. An alveolus of larger radius requires correspondingly lower pressure to overcome surface tension eliminating the need for lung surfactants 200 mg avana. However, the cornea, which is the transparent surface layer of the eye, does not contain blood vessels (this allows it to be transparent). The cells in the cornea receive oxygen by diffusion from the surface layer of tear fluid, which contains oxygen. This fact allows us to understand why most contact lenses should not be worn during sleep. Of course, when people sleep they do not blink; therefore, the corneas under their contact lenses are deprived of oxygen. Fish using air bladders to control their buoyancy are less stable than those using porous bones. A scuba diver breathes air from a tank which has a pressure regulator that automatically adjusts the pressure of the inhaled air to the ambient pressure. If a diver 40 m below the surface of a deep lake fills his lungs to the full capacity of 6 liters and then rises quickly to the surface, to what volume will his lungs expand? Assume that the average velocity of the molecules is 104 cm/sec and that the mean free path is 10−8 cm. Show that if the oxygen requirement of an animal is reduced by a factor of 10, then within the same lung volume, alveolar radius can be increased by a factor of 10. Chapter 10 T herm odynam ics Thermodynamics is the study of the relationship between heat, work, and the associated flow of energy. After many decades of experience with heat phenomena, scientists formulated two fundamental laws as the foundation of thermodynamics. The First Law of Thermodynamics states that energy, which includes heat, is conserved; that is, one form of energy can be converted into another, but energy can neither be created nor destroyed. Perhaps the simplest state- ment of the Second Law of Thermodynamics is that spontaneous change in nature occurs from a state of order to a state of disorder. In 1840 Mayer was the physician on the schooner Java, which sailed for the East Indies. While aboard ship, he was reading a treatise by the French scientist Laurent Lavoisier in which Lavoisier suggested that the heat produced by animals is due to the slow combustion of food in their bodies. Lavoisier further noted that less food is burned by the body in a hot environment than in a cold one. He noticed that the venous blood, which is normally dark red, was nearly as red as arterial blood. Because in the tropics less fuel is burned in the body, the oxygen content of the venal blood is high, giving it the brighter color. Mayer then went beyond Lavoisier’s theory and suggested that in the body there is an exact balance of energy (which he called force). The energy released by the food is balanced by the lost body heat and the work done by the body. Mayer wrote in an article published in 1842, “Once in existence, force [energy] cannot be annihilated— it can only change its form. Conservation of energy is implicit in all our calculations of energy balance in living systems. The body of an animal contains internal thermal energy Et, which is the product of the mass and specific heat, and chemical energy Ec stored in the tissue of the body. In terms of energy, the activities of an animal consist of simply eating, working, and rejecting excess heat by means of various cooling mechanisms (radiation, convection, etc. Without going into detailed calculations, the first law allows us to draw some conclusions about the energetics of the animal. For example, if the internal temperature and the weight of the animal are to remain constant (i. An imbalance between intake and output energy implies a change in the sum Ec + Et. The First Law of Thermodynamics is implicit in all the numerical calculations presented in Chapter 11. For example, when an object falls from a table to the ground, its potential energy is first converted into kinetic energy; then, as the object comes to rest on the ground, the kinetic energy is converted into heat. The First Law of Thermodynamics does not forbid the reverse process, whereby the heat from the floor would enter the object and be converted into kinetic energy, causing the object to jump back on the table. The irreversibility of these types of events is intimately connected with the probabilistic behavior of systems comprised of a large ensemble of subunits. Suppose that we now shake the tray so that each coin has an equal chance of landing on the tray with either head or tail up. Of these, only one yields the original ordered arrangement of three heads (H,H,H). Because the probabilities of obtaining any one of the coin arrangements in Table 10. As the number of coins in the experiment is increased, the probability of returning to the ordered arrangement of all heads decreases. With 10 coins on the tray, the probability of obtaining all heads after shaking the tray is 0. We could shake the tray for many years without seeing the ordered arrangement again. In summary, the following is to be noted from this illus- tration: The number of possible coin arrangements is large, and only one of them is the ordered arrangement; therefore, although any one of the coin arrangements—including the ordered one—is equally likely, the probability of returning to an ordered arrangement is small. As the number of coins in the ensemble increases, the probability of returning to an ordered arrangement decreases. In other words, if we disturb an ordered arrangement, it is likely to become disordered. This type of behavior is characteristic of all events that involve a collective behavior of many components. The Second Law of Thermodynamics is a statement about the type of prob- abilistic behavior illustrated by our coin experiment. One statement of the second law is: The direction of spontaneous change in a system is from an arrangement of lesser probability to an arrangement of greater probability; that is, from order to disorder. This statement may seem to be so obvious as to be trivial, but, once the universal applicability of the second law is recognized, its implications are seen to be enormous. We can deduce from the second law the limitations on information transmission, the meaning of time sequence, and even the fate of the universe. One important implication of the second law is the limitation on the con- version of heat and internal energy to work. This restriction can be understood by examining the difference between heat and other forms of energy. Yet when we examined the details of this energy transfer, we saw that it could be attributed to transfer of a specific type of energy such as kinetic, vibrational, electromagnetic, or any combination of these (see Chapter 9). It is, in fact, possible to develop a theory of thermodynamics without using the con- cept of heat explicitly, but we would then have to deal with each type of energy transfer separately, and this would be difficult and cumbersome. In many cases, energy is being transferred to or from a body by different methods, and keeping track of each of these is often not possible and usually not necessary. The main feature that distinguishes heat from other forms of energy is the random nature of its manifestations. Similarly, when heat is transferred by radiation, the propagating waves travel in random directions. The radiation is emitted over a wide wavelength (color) range, and the phases of the wave along the wave front are random. Chemical energy, for example, is present by virtue of specific arrangements of atoms in a molecule. Potential energy is due to the well-defined position, or configuration, of an object. While one form of energy can be converted to another, heat energy, because of its random nature, cannot be completely converted to other forms of energy. First, let us examine how heat is converted to work in a heat engine (for example, the steam engine). Heat flows into the gas; this increases the kinetic energy of the gas molecules and, therefore, raises the internal energy of the gas. The molecules moving in the direction of the piston collide with the piston and exert a force on it. The heat added to the gas causes the molecules in the cylinder to move in random directions, but only the molecules that move in the direction of the piston can exert a force on it. Therefore, the kinetic energy of only the molecules that move toward the piston can be converted into work. For the added heat to be completely converted into work, all the gas molecules would have to move in the direction of the piston motion. The odds against the complete conversion of 1 cal of heat into work can be expressed in terms of a group of monkeys who are hitting typewriter keys at random and who by chance type out the complete works of Shakespeare without error. Although some of the random thermal motion can be ordered again, the ordering of all the motion is very improbable. Because the probability of completely converting heat to work is vanishingly small, the Second Law of Thermodynamics states categorically that it is impossible. Heat can be partially converted to work as it flows from a region of higher temperature T1 to a region of lower temperature T2 (see Fig. A quanti- tative treatment of thermodynamics shows (see, for example, [11-5]) that the maximum ratio of work to the input heat is Work T2 1 − (10. From this equation, it is evident that heat can be completely converted into work only if the heat is rejected into a reservoir at absolute zero temperature. Although objects can be cooled to within a very small fraction of absolute zero, absolute zero cannot be attained. In fact, the first law could lead us to the erroneous conclusion that animals should be able to function without a source of external energy. The body takes in energy that is in the chemical bonds of the food molecules and converts it to heat. If the weight and the temperature of the body remain constant and if the body performs no external work, the energy input to the body equals exactly the heat energy leaving the body. We may suppose that if the heat outflow could be stopped—by good insulation, for example—the body could survive without food. The need for energy is made apparent by examining the functioning of the body in the light of the Second Law of Thermodynamics. A single protein molecule in the body may consist of a million atoms bound together in an ordered sequence. Their specialized functions within the body depend on a specific structure and location. We know from the Second Law of Thermodynamics that such a highly ordered system, left to itself, tends to become disordered, and once it is disordered, it ceases to function. For example, the blood circulating in veins and arteries is subject to friction, which changes kinetic energy to heat and slows the flow of blood. The concentration of minerals inside a cell differs from that in the surrounding environment. Finally, cells that die must be replaced, and if the animal is growing, new tissue must be manufactured. For such replacement and growth, new proteins and other cell constituents must be put together from smaller, relatively more random subcomponents. Thus, the process of life consists of building and maintaining ordered structures. The situation is somewhat analogous to a pillar made of small, slippery, uneven blocks that tend to slide out of the structure. The work necessary to maintain the ordered structures in the body is obtained from the chemical energy in food. Except for the energy utilized in external work done by the muscles, all the energy provided by food is ulti- mately converted into heat by friction and other dissipative processes in the body. Once the temperature of the body is at the desired level, all the heat generated by the body must leave through the various cooling mechanisms of the body (see Chapter 11). The heat must be dissipated because, unlike heat engines (such as the turbine or the steam engine), the body does not have the ability to obtain work from heat energy. Even if the body did have mechanisms for using heat to perform work, the amount of work it could obtain in this way would be small. The temperature differences in the body are small—not more than about 7 C◦ between the interior and the exterior. With the interior temperature T at 310 K (37◦C) and the exterior 1 temperature T1 at 303 K, the efficiency of heat conversion to work would be (from Eq.

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While the amount of noradrenaline released from the terminals can be increased by nerve stimulation avana 200mg, it can be increased much more by drugs avana 50mg, like phenoxybenzamine avana 100 mg, which block presynaptic a-adrenoceptors 100mg avana. These presynaptic autoreceptors play an important part in ensuring that transmitter stores are conserved and preventing excessive stimulation of the postsynaptic cells 200mg avana. Pharmacological characterisation of this receptor revealed that it was unlike classic a-adrenoceptors found on smooth muscle 100 mg avana. In particular 50mg avana, receptors modulating noradrenaline release have a higher affinity for the agonist 200 mg avana, clonidine avana 100mg, and the antagonist 50 mg avana, yohimbine. This distinctive pharmacology led to the subdivision of a-adrenoceptors into the a1- and the a2-subtypes. Although the latter is the subtype responsible for feedback inhibition of noradrenaline release, the majority of a2-adrenoceptors are actually found postsynaptically in some brain regions. There is still some debate over the identity of the subtype of a2-adrenoceptors responsible for feedback inhibition of transmitter release. However, most studies agree that the a2A/D-subtype has the major role, although the a2B-anda2C-subtypes might contribute to this action. Species differences in the relative contributions of these different receptors are also possible. Itisa2A-adrenoceptors that are found on cell bodies of noradrenergic neurons in the locus coeruleus. Whichever of these release- controlling processes predominates is uncertain but it is likely that their relative importance depends on the type (or location) of the neuron. The precise role of these receptors in regulation of noradrenaline release in vivo is uncertain because noradrenaline has a relatively low affinity for these receptors. However, one suggestion is that, in the periphery, they are preferentially activated by circulating adrenaline which has a relatively high affinity for these receptors. This activation could enable circulating adrenaline to augment neuronal release of noradrenaline and thereby effect a functional link between these different elements of the sympathoadrenal system. However, the extent to which this actually happens is uncertain as is a physiological role for b-adrenoceptors in regulation of nor- adrenaline release in the brain. A further possible mechanism, that would enable different types of neurons to modify noradrenaline release, is suggested by recent in vitro studies of brain slices. There is no doubt that this form of release depends on vesicular exocytosis because it is Ca2‡-dependent, sensitive to tetrodotoxin and, like impulse- dependent release, it is attenuated by a2-adrenoceptor agonists (see above). The extent to which this process occurs under normal physiological conditions in vivo remains to be seen. This uptake process relies on membrane-bound noradrenaline transporters which are glycoproteins closely related Figure 8. Binding domains for specific ligands are thought to be within regions indicated by the solid bars. The hypothetical structure of the noradrenaline transporter is illustrated in Fig. Because co-transport of both Cl7 and Na‡ is required for the uptake of noradrenaline, this is regarded as one of the family of Na‡/Cl7 transporters. Exactly how this transporter carries noradrenaline across the neuronal membrane is not known but one popular model proposes that it can exist in two interchangeable states. This process enables the translocation of noradrenaline from the extracellular space towards the neuronal cytosol. Point-mutation and splicing studies indicate that different zones of the transporter determine its substrate affinity and selectivity, ionic dependence, Vmax, and the binding site for uptake inhibitors such as desipramine (Povlock and Amara 1997). Because the cloned transporter is a target for the reuptake inhibitor, desipramine, it is thought to reflect the native transporter in the brain and peripheral tissues. These are quite distinct uptake mechanisms because they have different substrate affinities and antagonist sensitivities. At the very least, intracellular messengers could modify substrate affinity of the transporter, by causing its phosphorylation or glycosylation (Bonisch, Hammermann and Bruss 1998), and so markedly affect its function. Whether or not there are different gene products, splice variants, or posttranslational changes, it has been suggested that abnormal distributions of functionally distinctive noradrena- line transporters could underlie some psychiatric and neurological disorders. The metabolic pathway for noradrenaline follows a complex sequence of alternatives because the metabolic product of each of these enzymes can act as a substrate for the other (Fig 8. This could enable one of these enzymes to compensate for a deficiency in the other to some extent. Certainly, such a complex system for metabolism of noradrenaline (which is shared with the other catecholamines) strongly suggests that its function extends beyond that of merely destroying transmitter sequestered from the synapse. However, as yet, little is known about the regulation of this pathway and any influence it might have on noradrenergic transmission. Its predominantly intraneur- onal location would suggest that its primary function is to ensure that there is always a low concentration of cytoplasmic noradrenaline. What can happen when the concentration of cytosplasmic noradrenaline is increased is illustrated by amphetamine. This drug causes a rise in the cytoplasmic noradrenaline and results in increased binding of this transmitter to the cytoplasmic side of the transporter which then carries it out of the neuron. When this enzyme is inhibited, the amount of noradrenaline held in the vesicles is greatly increased and there is an increase in transmitter release. These drugs are proving to be highly effective antidepressants which avoid the need for a tyramine-free diet. Although many of these compounds are potent and selective a2-adrenoceptor ligands (e. It is now known that many of these drugs have their own binding sites that are now classified as imidazoline (I-) receptors. Further subdivision of b-adrenoceptors followed characterisation of their distinctive actions in the heart (b1), where they enhance the rate and force of myocardial contraction and in the bronchi (b2), where they cause relaxation of smooth muscle. The binding profile of selective agonists and antagonists was the next criterion for classifying different adrenoceptors and this approach is now complemented by molecular biology. The development of receptor-selective ligands has culminated in the characterisation of three major families of adrenoceptors (a1, a2 and b), each with their own subtypes (Fig. All these receptors have been cloned and belong to the superfamily of G-protein-coupled receptors predicted to have seven transmembrane domains (Hieble, Bondinell and Ruffolo 1995; Docherty 1998). The a1-subgroup is broadly characterised on the basis of their high affinity for binding of the antagonist, prazosin, and low affinity for yohimbine but they seem to be activated to the same extent by catecholamines. There are at least three subtypes which for historical reasons (Hieble, Bondinell and Ruffolo 1995) are now designated a1A, a1B and a1D. An alternative classification (also based on sensitivity to prazosin) characterised two classes of receptor: a1H and a1L receptors. Whereas those classified as a1H seem to overlap with a1A, a1B and a1D receptors (and are now regarded as the same), there is no known equivalent of the a1L receptor. Although it is still tentatively afforded the status of a separate receptor, it has been suggested that it is an isoform of the a1A subtype (Docherty 1998). All a1-adrenoceptors are coupled to the Gq/11 family of G-proteins and possibly other G-proteins as well. These include: direct coupling to Ca2‡ (dihydropyridine sensitive and insensitive) channels, phospholipase D, phospholipase A2, arachidonic acid release and protein kinase C. All three subtypes are found throughout the brain but their relative densities differ from one region to another. A detailed review of the classification of a1-adrenoceptors is to be found in Zhong and Minneman (1999). However, stimulatory effects of a2-adrenoceptors have also been reported, although the underlying mechanisms are unclear. Paradoxically, the different receptor subtypes are characterised by their affinity for prazosin: the a2A-subtype (found in human platelets) has a low affinity for this ligand, while the a2B-subtype (isolated from neonatal rat lung) has a higher affinity. This has not been granted the status of a separate subtype, partly because it has not been possible to produce a distinctive receptor clone, and it is now regarded as the rodent homologue of the human a2A-subtype. It is the a2A/D-adrenoceptor that predominates in the locus coeruleus and this subtype seems to be responsible for reducing neuronal excitability and transmitter release. Strangely, immunocytochemical studies suggest that most a2C-receptors are intracel- lular. The explanation for this finding and its functional implications are as yet unknown but it could reflect differences in intracellular trafficking of different receptor subtypes. Unlike b1- and b2-adrenoceptors, this subtype is not found in the brain but probably has an important role in lipolysis by mobilising triglyceride stores and promoting thermogenesis (Giacobino 1995). In the brain, autoradiography has shown that b1-andb2-adrenoceptors have quite distinct distributions. As yet, the functional implications of this uneven distribution are unclear and await the development of more subtype selective agents. However, unlike the a-adrenoceptor families, the affinity of catecholamines for b-adrenoceptors differs markedly: noradrenaline is a relatively weak agonist at the b2-subtype whereas it is more potent than adrenaline at b3-receptors. Electrophysiological studies of the b-adrenoceptor have produced complex findings. In cardiac tissue, their activation leads to an increase in Ca2‡ conductance and so they are regarded as excitatory receptors. A different response is evoked in thalamic relay neurons where these receptors cause depolarisation and an increase in input conductance by resetting a hyperpolar- isation-induced cation current. In the dentate gyrus their activation causes an increase in voltage-dependent Ca2‡ currents through opening of Ca2‡ channels. Because of these disparate findings, it is difficult to assign particular electro- physiological changes to each of the adrenoceptors let alone to noradrenaline, more generally. Another difficulty concerns the uncertain location of the receptors responsible for initiating any changes. In tissue slices, the target receptors could be located on interneurons, rather than mediating direct axo-somatic interactions, for instance. The net effect of receptor activation could also depend on the underlying tonic activity of the target cell as well as the influence of other neurotransmitters that converge on the same G-protein. Despite these obstacles, it has been suggested that the overall effect of interactions between noradrenaline and its receptors could be to increase the excitability and responsiveness of the target cells. This could make an important contribution to the governance of arousal and selective attention (McCormick, Pape and Williamson 1991). Another, similar suggestion is that noradrenergic transmission increases the signal-to-noise ratio of cell responses to incoming stimuli: i. Because central noradrenergic pathways are so diffuse, and the synaptic effects of noradrenaline have a comparatively slow time-course, these neurons could have a wide range of functions, depending on the brain region being targeted and the neurobiological status of the individual. In general terms, however, it is agreed that noradrenergic neurons influence arousal. This encompasses not only the sleep/waking cycle (see Chapter 22) but also more specific activities, such as selective attention and vigilance (Aston-Jones et al. Indeed, depression and anxiety, both of which are relieved by drugs that modify noradrenergic transmission, can be regarded as arousal disorders. Yet, despite nearly 40 years of research, it is still uncertain whether an increase in noradrenergic transmission contributes to unpleasant emotional responses to environmental stimuli (e. Many electrophysiological studies have shown that single-unit activity of noradrenergic neurons in the locus coeruleus is increased by sensory stimuli. This would be consistent with the attenuation of the neuronal response on repeated presentation of the test stimulus, the presumption being that this change underlies behavioural habituation. Even if this turns out to be the case, it is likely that noradrenergic neurons in different brain regions make different contributions to this process. This complication is suggested by the results of a recent microdialysis study in which release of noradrenaline in response to the sound of a buzzer alone was provoked after repeated Figure 8. This adaptive change occurred in the frontal cortex but not the hypothalamus suggesting that only noradrenergic neurons innervating the former brain region (i. Another concept is that noradrenergic transmission influences the emotional impact of a given stimulus, i. One obvious possibility is that inadequate noradrenergic transmission explains depression, whereas moderate activity provokes attentive interest that is vital for appropriate cognitive function, and excessive noradrenergic activation culminates in anxiety or agitation. Evidence supporting this single axis for central noradrenergic function/dysfunction is discussed in Chapters 19 and 20. It is equally possible that the role and consequences of central noradrenergic transmission depend on the type or severity of the stimulus and individual differences in the neurobiological coding of behaviour. This would mean that the optimal behavioural response to a given environmental stimulus requires a specific increase in noradrenergic transmission. However, it is also possible to envisage disruption of this neurochemical coding of behaviour in the ways illustrated in Figs 8. If there is a shift of the curve to either the right or the left, then the noradrenergic response that would be optimal in normal subjects now produces a suboptimal coping response. In the case of a shift to the left, a reduction in noradrenergic transmission would be required to restore optimal coping whereas for a shift to the right, an increase would be required. One is that the underlying coding is correct but it is the noradrenergic response evoked by the stimulus that is inappropriate. A second is that the amplitude of the noradrenergic response to arousing stimuli is normal but the underlying coding is not. For instance, an early report suggested that there is a positive correlation between the density of (postsynaptic) b-adrenoceptors in rat cortex and behavioural resistance to a mild environmental stress (novelty and frustration) but a negative correlation between these parameters when the stress is intensified (Stanford and Salmon 1992). Evidence suggests that the relationship between these two parameters is described by a bell-shaped curve and so an optimal phasic response is manifest only at intermediate levels of tonic activity (Rajkowski et al. Obviously, it is extremely unlikely that noradrenergic transmission is the sole factor to determine the behavioural response to even simple environmental stimuli. Indeed, a bell-shaped dose±response curve immediately suggests the intervention of one or more additional factors (neurotransmitters? Such interactions with other neurotransmitters could well define the relationship between noradrenergic transmission and the coding of the coping response.

All B vitamins help oxidize food avana 200mg, something for which cancer sufferers have reduced capa- bility 100 mg avana, causing fatigue 100mg avana. It can detoxify phenol to magnesium phenyl phosphate avana 100mg, allowing it to leave through the kidneys 50 mg avana. The green drinks on page 549 can supply some and do not pose a pollution risk nor aggravate diarrhea 200 mg avana. Choline avana 200 mg, too avana 100 mg, is easily obtained from food 50mg avana, so there is no need to risk taking a tablet or capsule avana 50mg. Ornithine and Arginine, both 500 mg, are very important detoxifiers of ammonia via the urea synthesis cycle. If you get a few drops on your skin it may turn white and sting, but does no harm, so simply wash it off. If the herbs are in capsules you must test for petroleum pollution (benzene and other solvents). Don’t purchase extracts or con- centrates because they are invariably polluted (unless you can test them, of course). It is made this way be- cause plain iodine does not dissolve well in water; it dissolves much better in potassium iodide. Potassium iodide dissolves well in water and stays clear; for this reason it is also called “white iodine. You can become allergic from having a large amount of iodine poured into you during a special clinical thyroid or kidney procedure. The amount you use is immediately hung up, or attached, to your mucous and can not be quickly absorbed into the blood or other organs. They can give you terrible bloating and gas which is often misdiagnosed as lactose intolerance. It comes into you with deli food, chicken, dairy food, not to mention picnic food that has stood around for a while. Every new strain they eat or drink evidently forms hybrids with the old strain they already had in their stom- achs. Shigella, especially, makes you feel angry, irritable, and short-tempered as a mule. Take this dose 4 times a day, after meals and at bedtime, for 3 days in a row, then daily at bedtime. Doomed are Salmonella and other local bacteria; doomed also are eggs (cysts) of parasites that might be in the stomach. Amazingly, the two teaspoon dose of Black Walnut Hull Tincture Extra Strength used in the Parasite Killing Program is also effective against many bacteria, including Salmonella, Shi- gella, and Clostridium. If the tincture doesn’t bring total relief in 24 hours, search for a source of reinfection. These bacteria come to us in dairy foods, or perhaps you are self infecting by putting your fingers in your mouth. A traditional, more gradual method of conquering digestive bacteria is with two herbs (which are also common spices! Another traditional treatment for digestive problems is yo- gurt and acidophilus beverages. But modern commercial varie- ties are actually contaminated with Salmonella and Shigella strains. The concept of supplementing the diet is excellent, but the pollution problem makes it prohibitive. This is an easy task because it mostly involves throwing things out, so it was left to the last. Special Clean-up For Freon Your refrigerator is the most sinister toxin in your home! But switching to Freon as a refrigerant, which is nearly odorless, brought a new threat: unsuspected leakage. You may leave it on an extension cord and use it until you find a new non-Freon variety. Although everybody in the health profes- sions know this, it is never discussed in scientific circles. Perhaps morbitropism has a magnetic or electronic explanation, and will soon be a legitimate subject for study. Would Freon react with ozone supplied to your body and thereby become biodegradable? Other ozone routes, as intravenous or rectal, have not been observed to be as effective. Drink three glasses a day for the first week, then two glasses a day for six more weeks. A combination of herbs (Liver Herbs in Recipes, page 599) rescues the liver from its plight, and prevents the indigestion. After drink- ing liver herbs you will see that the Freon now appears in the kidneys. Take the kidney cleanse (page 596) to assist the kidneys so they can finally excrete the Freon into the urine. It’s an elaborate detoxifying program of ozonated water, liver herbs, and kidney herbs taken together for six to eight weeks. Although toxic, at least I observe it in the liver directly, suggesting that your body is capable of handling it. Remember your new refrigerator will still be using a toxic coolant, and it would be best to keep it out- side or at least vented to the outside. You must test a dust sample taken from a flat surface in your car or home (after changing your refrigerator) to find out if it is leaking. Fortunately, the success rate on fixing air condi- tioners is quite good, in contrast to fixing refrigerators. If you are very sick, find a home without air conditioners and move the refrigerator outside. They cut their way through your lungs and organs like millions of tiny knives, spreading through your body, since there is no way out for them. Your body, though, recognizes these sharp, pointed bits and tries to stop their spread by sequestering them in cysts. Most solid malignant tumors contain fiberglass or asbestos, another glass-like particle. In nearly all cases a hole can be found in the ceiling or walls, leading to fiberglass insulated parts of the house. When these holes are sealed in an air-tight manner the house air no longer is positive for fiberglass. Search for small screw holes intended for pictures, or electric outlet plates that are missing. Also remove fiberglass jackets from your water heater and fiberglass filters from your furnace and air conditioner. Best of all, hire a crew to remove it all from your home, and replace insulation with blown-in shredded paper or other innocuous substance. Clean Basement To clean your basement, remove all paint, varnish, thinners, brush cleaners, and related supplies. You may keep your laundry supplies: borax, white distilled vinegar, chlorine bleach and homemade soap. Also move any car tires and automotive supplies like waxes, oil, transmission fluid, and the spare gas can (even if it is empty) into your garage or dis- card them. Seal cracks in the basement and around pipes where they come through the wall with black plastic roofing cement. Tack a sheet of plastic over it to slow down the rate of fume entrance into the house. Your house is taller and warmer than the garage so garage-air is pulled in and up as the warm air in the house rises. But what of the gasoline and motor fumes we are getting now due to parked vehicles? Remove every- thing that has any smell to it whatever: candles, potpourri, soaps, mending glue, cleaners, repair chemicals, felt markers, colognes, perfumes, and especially plug-in air “fresheners”. Since all vapor rises, they would come back up if you put them in a downstairs garage or basement. Keep only the borax, white distilled vinegar and bottles of concentrated borax and 50% vinegar you have made. Remove all cans, bottles, roach and ant killer, mothballs, and chemicals that kill insects or mice. A cancer patient should not be in the house while house cleaning or floor waxing is being done. To keep out mice, walk all around your house, stuffing holes and cracks with steel wool. Use vinegar on your kitchen wipe-up cloth to leave a resi- due that keeps out ants. Pour vinegar all around your house out- side, using one gallon for every five feet, to deter ants. Family members should buy unfragranced products which must not contain isopropyl alcohol. They should smoke outdoors, blow-dry their hair outdoors or in the garage, use nail polish and polish remover outdoors or in the garage. If other rooms have paneling or wall- paper, close their doors and spend no time in them. Take taurine and cysteine to help your body recover from formaldehyde damage (same dosages as given on page 170). Because it looks like sugar, keep it in the garage, la- beled, to prevent accidental poisoning. Do not use the hot water from an electric hot water heater for cooking or drinking. Do not drink water that sits in glazed crock ware (the glaze seeps toxic elements like cadmium) like some water dispensers have. All holding tanks, all stills, all pumps, must be periodically cleaned, sterilized and greased. It would be interesting to find out who is servic- ing your health food store’s supply and with what. It would be wise to switch to plastic plumbing before anybody in your home develops illnesses. If you have a water softener, by-pass it immediately and re- place the metal pipe on the user side of the softener tank. Sof- tener salts are polluted with strontium and chromate; they are also full of aluminum. After changing your pipes to plastic, there will be so little iron and hardness left, you may not need a softener. If you must have softening after all this, check into the new magnetic varieties of water softener (although they only work well when used with plastic plumbing). The coating hardens in a day; it did not appear in the white blood cells later when I tested with the Syncrometer. If you must stay with gas, have a furnace repair person check your furnace and look for gas leaks before the heating season starts. Suppose you have nobody who is willing to clean up the house, basement, garage for you, or take on your pets for a month while you find them a new home. Remember not to use any sunscreen or suntan lotions; make your own (see Recipes) or simply wear a hat. Notice from the case histories how isopropyl alcohol disappears from the body simply by removing the sources. You are no longer sucking on copper, cobalt, vanadium, malonic and maleic acid, urethane or scarlet red dye. This means foods that are fresh and have not been chopped, ground, extracted and mixed with other chopped, ground, extracted foods to create concoc- tions. You have stopped using supplements unless you know they have been tested for isopropyl alcohol pollu- tion. I hope you did all this in the first week after you bought this book and started on the parasite killing program. If you have had three weeks of this healthful lifestyle, you should ask your doctor for a fresh evaluation of your situation. If lumps are going down or pain is reduced, tell your doctor about this, so he or she has some basis for giving you a postponement. If a new specimen is taken from you for testing, it may be evaluated by the lab as “questionable” or “indeterminate” or “atypical” but not “definite”, like before. Wait for this to happen rather than approving a surgery that could handicap you for life. Since the infective stage in nature is 54 the metacercarial stage, are we eating metacercaria from vegetation like lettuce? I have not seen evidence for this but it must be researched, thoroughly, as a possibility. In cases of persistent reinfection the pa- tient either had family members who were infected (although symptom-free), or they had repeatedly indulged in fast foods or delicatessen meats. Parasites can make good progress in two days (eating you up and reproducing in you) if given the chance. Unfortunately for fast food lovers, the solution is not to make a daily routine out of the maintenance program. Herbs powerful enough to kill parasites probably are not advisable on a daily basis. The metacercaria are meant to attach themselves to our in- testine and grow larger, into adults that lay more eggs.

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