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By X. Lester. Alabama State University. 2019.

Patients experienced a decline in life-threatening morbidities and an overall improvement in survival cheap 100 mg zudena, showing conclusively that eculizimab has become a very effective treatment for a previously unmet need buy generic zudena 100mg online. Parker cheap 100 mg zudena with visa, Hematology/the Education Program of the American Society of Hematology order zudena 100 mg amex, American Society of Hematology, Education Program, 2008, pp. The challenge for a small group of scientists, comprising 20–30 chemists and an equal number of biologists, was to identify compelling therapeutic targets in the chosen disease indications that offered opportunities to discover rst-in-class or well-differentiated molecules with superior pharmacological, pharmaceu- tical and/or toxicological properties compared with competitor compounds. Incyte scientists began a comprehensive survey of druggable targets in the chosen therapeutic areas, assessed the strength of the pre-clinical and clin- ical evidence supporting the targets, evaluated the competitive landscape, and prioritised the targets based on a number of internally established criteria. View Online The Discovery and Development of Ruxolitinib for the Treatment of Myelobrosis 421 15. View Online 422 Chapter 15 the nucleus to initiate the transcription of genes involved in the promotion of cell growth, proliferation, differentiation and survival, as well as cytokine and growth factor expression. The pathway is normally activated by growth factor and cytokine receptor stimulation and participates in cytokine signalling and haematopoiesis. Symptoms include fatigue, night sweats, fever, itching (pruritus), abdominal discomfort, pain under le ribs, early satiety, weight loss and bone/muscle pain,29,32 and it negatively impacts patient QoL. Splenomegaly is associated with abdominal discomfort and pain and leads to poor nutritional status, cachexia and low cholesterol. Patients with 0 risk factors have low-risk disease; the addition of one risk factor changes the classication to intermediate-1 risk; the presence of two risk factors changes the classica- tion to intermediate-2 risk; and high-risk patients have three or more risk factors. Treatments included hydroxyurea, corticosteroids, thalidomide, lenalidomide, ana- grelide, epoetin alfa and danazol. Additional treatment options for splenomegaly are splenic irradiation and splenectomy, but they are associated with cytopenias, and splenectomy carries risks of perioperative complications and mortality. Selection of ruxolitinib as a development candidate was based on in vitro and in vivo pharmacology data, its pharmacokinetic prole and toxicology data, described in part below. It exists as a white to off-white to light pink powder, and it is soluble in aqueous buffers ranging from pH 1 to 8. Ruxolitinib tablets contain ruxolitinib phosphate, along with microcrystalline cellulose, lactose monohydrate, magnesium stearate, colloidal silicon dioxide, sodium starch glycolate, povidone and hydrox- ypropyl cellulose. Testing against 26 additional kinases showed no inhibition by ruxolitinib when used at Figure 15. View Online The Discovery and Development of Ruxolitinib for the Treatment of Myelobrosis 427 Table 15. No myelosuppressive or immunosuppressive effects were seen in ruxolitinib- treated mice. Rapid and almost complete (96%) absorption was observed, and maximum serum concentra- tions (C ) were reached in 1–2 hours. Excretion is primarily renal, as 74% of a single 25 mg radio- labelled dose administered to healthy subjects was recovered in urine, and 22% was recovered in faeces. Patients with enlarged spleens at study entry were evaluated over a 3 month period to determine the proportion achieving a $50% reduction in palpable spleno- megaly. Overall, spleen size reductions were rapid and durable, occurring in most patients within the rst 1–2 months and lasting for approximately 2 years. Patients with reductions in spleen size reported reductions in abdominal discomfort. Heat maps were constructed to show the differences in plasma levels of each of these factors for individual patients at baseline versus healthy controls and also for individual patients at day 28 versus baseline (Figure 15. Levels of erythropoietin and leptin, which were below normal at baseline, increased aer ruxolitinib treatment. Non-haematological toxicities occurred at an incidence of <10% and were of low grade. The main haema- tological toxicities were new-onset anaemia in patients who were transfusion- independent at baseline (23%) and dose-limiting grade 3 or 4 thrombocy- topenia (20%). Aer an initial decrease in mean haemoglobin levels over the rst three to four cycles of therapy, levels stabilised or improved from the nadir with subsequent therapy. Green indicates markers present at lower levels at baseline and markers that decreased with ruxolitinib treatment. Red indicates markers present at higher levels at baseline and markers that increased with ruxolitinib treatment. As of September 2013, the long-term extension phases of both trials remain ongoing. Aer 24 weeks of treatment, signicantly more patients achieved a $35% reduction in spleen volume from baseline with ruxolitinib (41. Almost all patients who received ruxolitinib had reductions in spleen volume at week 24; in contrast, most patients who received placebo had increases or no change in spleen volume. While almost all patients who received ruxolitinib experienced some decrease in spleen volume, the majority of patients in the placebo group experienced increases in spleen volume over the 24 week period (Figure 15. Of the ruxolitinib-treated patients with a $35% reduc- tion in spleen volume, 67% maintained this reduction for at least 48 weeks. Most symptom improvements with ruxolitinib occurred within the rst 4 weeks of treatment and were maintained through week 24. At week 24, patients who received ruxolitinib treatment showed decreases in these pro-inammatory cytokines, while patients who received placebo had minimal changes. Plasma levels of leptin and erythropoietin increased by week 24 in rux- olitinib-treated patients and showed no or minimal change in patients who received placebo. These events generally occurred early in the course of therapy and were managed with red blood cell transfusions and dose adjustments/treatment View Online The Discovery and Development of Ruxolitinib for the Treatment of Myelobrosis 433 interruptions, respectively. Non-haematological events generally occurred at similar frequencies in both treatment groups. Ecchymosis, dizziness and headache occurred more frequently in the ruxolitinib group and were mainly grade 1 or 2. Secondary end points included the proportion of patients who achieved a $35% spleen volume reduction from baseline at week 24, duration of reduction of spleen volume $ 35%, and time to reduction in spleen volume $ 35%. The median duration of reduction in spleen volume $ 35% was not reached, as 80% of patients had maintained their response at 12 months, and the median time to spleen volume reduction $ 35% was 12. A greater proportion of ruxolitinib-treated patients achieved stabilisation or improvement of brosis grade at 24 and 48 months compared with patients who received hydroxyurea (at 24 months, 72% with ruxolitinib versus 62% with hydroxyurea; at 48 months, 77% with ruxolitinib versus 35% with hydroxyurea). Patients who received hydroxyurea had greater worsening of bone marrow brosis grade at both time points. Acknowledgements The author would like to thank Stephanie Leinbach, PhD, for editorial assistance. View Online The Discovery and Development of Ruxolitinib for the Treatment of Myelobrosis 437 18. James, Hematology/the Education Program of the American Society of Hematology, American Society of Hematology, Education Program, 2008, p.

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Raman spectroscopy Same as conventional Raman spectroscopy purchase zudena 100mg without a prescription, Moderate Low Fast Yes Falsifed artesunate samples did not produce the strong (portable) but can be less reliable fuorescence characteristic of artesunate when scanned with a portable device (Ricci et al generic zudena 100 mg otc. High-performance liquid Identifying and quantifying active Expensive High Slow No Distinguished between falsifed and genuine samples of chromatography-mass ingredients generic 100mg zudena visa, excipients zudena 100 mg lowest price, undeclared Nigerian dihydroartemisinin (Kaur et al. Artemisinin is sometimes substituted for its and tablet coatings derivatives, such as artemether, in falsifed products (Kaur et al. Near-infrared spectroscopy Identifying and quantifying active Moderate-expensive Moderate Fast Yes Was able to distinguish real from falsifed artesunate ingredients, excipients tablets with 100% accuracy in an analysis of samples from Southeast Asia (Dowell et al. Raman spectroscopy Identifying active ingredients and excipients, Moderate-expensive Moderate Fast No Close examination of Raman spectra comparing a (conventional) relative concentration of ingredients; suspected falsifed drug to a real sample revealed a identifying tablet coating composition slight discrepancy due to diferences in tablet coating (Witkowski, 2005). Raman spectroscopy Same as conventional Raman spectroscopy, Moderate Low Fast Yes Falsifed artesunate samples did not produce the strong (portable) but can be less reliable fuorescence characteristic of artesunate when scanned with a portable device (Ricci et al. High-performance liquid Identifying and quantifying active Expensive High Slow No Distinguished between falsifed and genuine samples of chromatography-mass ingredients, excipients, undeclared Nigerian dihydroartemisinin (Kaur et al. The emerging feld of medicines authentication by nuclear quadrupole resonance spectroscopy. Working paper: The impact of improved detection technology on drug quality: A case study of Lagos, Nigeria. Pilot study comparing technolo- gies to test for substandard drugs in feld settings. New technology represents next-generation tool for detecting substan- dard and counterfeit medicines. Poor quality drugs: Grand challenges in high throughput detection, coun- trywide sampling, and forensics in developing countries. Development and valida- tion of a reversed-phase lc method for analysing potentially counterfeit antimalarial medicines. Tanzanian food and drugs authority receives four unique mobile compact laboratories. Short communication: Authentication of artemether, artesunate and dihydroartemisinin antimalarial tablets using a simple colori- metric method. Use of refractometry and colorimetry as feld methods to rapidly assess antimalarial drug quality. Establishment of a fast chemical identifcation system for screen of counterfeit drugs of macrolide antibiotics. Ensuring safe foods and medical products through stronger regulatory systems abroad. Ofoxa- cin: Laboratory evaluation of the antibacterial activity of 34 brands representing 31 manufacturers available in Pakistan. A concise quality control guide on essential drugs and other medicines: Colour reaction tests. Paper read at 3rd Global Forum on Pharmaceutical Anticounterfeiting, Prague, Czech Republic. The quality of essential antimicrobial and antimalarial drugs marketed in Rwanda and Tanzania: Infuence of tropical stor- age conditions on in vitro dissolution. Detection of substandard fxed-dose combination tuberculosis drugs using thin-layer chromatography. Reliable low-cost capillary elec- trophoresis for drug quality control and counterfeit medicines. Analysis of organic volatile impurities as a forensic tool for the examination of bulk pharmaceuticals. A collaborative epidemiological investigation into the criminal fake artesunate trade in South East Asia. Combining two-dimensional diffusion-ordered nuclear magnetic resonance spectroscopy, imaging desorption elec- trospray ionization mass spectrometry, and direct analysis in real-time mass spectrom- etry for the integral investigation of counterfeit pharmaceuticals. Assessment of hand-held Raman instrumentation for in situ screening for potentially counterfeit artesunate antimalarial tablets by ft-Raman spectroscopy and direct ionizatoin mass spectrometry. Criteria for the identifcation of compounds by liquid chromatography-mass spectrometry and liquid chromatography-multiple mass spectrometry in forensic toxicol- ogy and doping analysis. Strategies for characterizing silde- nafl, vardenafl, tadalafl, and their analogues in herbal dietary supplements, and detect- ing counterfeit products containing these drugs. Multiple injection technique for the determination and quantitation of insulin formulations by capillary electrophoresis and time-of-fight mass spectrometry. High-performance liquid chromatographic method with diode array detection for iden- tifcation and quantifcation of the eight new antidepressants and fve of their active metabolites in plasma after overdose. Intelligence alert: Viagra® mimic tablet containing amphetamine in Fejer County, Hungary. Ensuring the quality of medicines in resource-limited coun- tries: An operational guide. Towards a decade of detecting new analogues of silde- nafl, tadalafl and vardenafl in food supplements: A history, analytical aspects and health risks. The use of Raman spectroscopy in the detection of counterfeit and adulterated pharmaceutical products. Identifcation of the “wrong” active pharmaceutical ingredient in a counterfeit Halfan™ drug product using accurate mass electrospray ionisation mass spectrometry, accurate mass tandem mass spectrometry and liquid chromatography/mass spectrometry. Countering the Problem of Falsified and Substandard Drugs 7 An International Code of Practice for Falsifed and Substandard Medicines Ensuring a safe, reliable drug supply is ultimately a matter for indi- vidual countries. To this end, every nation has four main responsibilities: regulating the responsible manufacture of safe and effective medicines; pre- venting falsifed and substandard drugs from entering the market; detecting them when they do; and punishing those who knowingly manufacture and trade them. Executing these responsibilities requires strong national systems for drug regulation, surveillance, and law enforcement. Governments must work with key stakeholders in industry, professional associations, and civil society to protect the drug supply. However, no country acting alone can protect its citizens from falsifed and substandard medicines. The problem, as seen throughout this report, is international, fueled by international trade and telecommunications. Crime and easy money are powerful forces driving the illegitimate medicines busi- ness. Its perpetrators gravitate to countries where surveillance, regulation, and law enforcement are the weakest. They take advantage of international manufacturing and trade to produce and sell their products in the global market. The interconnectedness of modern manufacturing systems makes the “quality and safety of goods. A coherent system of global governance founded on diplomacy and international co- operation can improve product safety and protect health around the world (Gostin and Taylor, 2008). This will require cooperation among countries, among agencies within governments, and among consumers, manufactur- ers, professional associations, and civil society groups. An emphasis on the public health risks of illegitimate drugs is central to framing this problem; protecting drug companies’ proprietary interests is not.

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Inject slowly over 3-4 minutes or in 100ml of compatible fluid over 30-40 minutes zudena 100mg without a prescription. Note that amoxicillin and clavulanic acid is less stable in solutions that contain glucose so these solutions should be avoided for intermittent infusions cheap zudena 100mg without a prescription. Amoxicillin and clavulanate potassium are well absorbed from the gastrointestinal tract after oral administration of Augmentin purchase zudena 100mg with visa. Clavulanic acid is active against the clinically important plasmid mediated beta-lactamases frequently responsible for transferred drug resistance to penicillins and cephalosporins zudena 100 mg overnight delivery. Amoxicillin is bactericidal against susceptible organisms during the stage of active multiplication. Amoxicillin/ clavulanic acid has been shown to be active against most strains of the following microorganisms, both in vitro and in clinical infections: Gram-Positive Aerobes: Staphylococcus aureus (beta-lactamase and non-beta-lactamase producing). Amoxicillin diffuses readily into most body tissues and fluids with the exception of the brain and spinal fluid. The results of experiments involving the administration of clavulanic acid to animals suggest that this compound, like amoxicillin, is well distributed in body tissues. Note: additional organisms (not outline above) which are adequately treated with amoxicillin alone should be treated with amoxicillin rather than augmentin. Therefore, it is important to consider this diagnosis in patients who present with diarrhoea subsequent to the administration of antibacterial agents. Hepatic dysfunction including cholestatic jaundice, hepatic cholestasis and acute cytolytic hepatitis have been reported. Nervous System: Reversible hyperactivity, agitation, anxiety, insomnia, confusion, convulsions, behavioral changes, and/or dizziness have been reported rarely. Skin: Stevens-Johnson Syndrome, exfoliative dermatitus, toxic epidermal necrolysis, acute generalized exanthematous pustulosis, hypersensitivity vasculitis and urticaria have been reported Haematological System: Anaemia, including haemolytic anaemia, thrombocytopaenia, thrombocytopaenic purpura, eosinophilia, leukopaenia, and agranulocytosis have been reported during therapy with penicillins. Suspected or proven fungal infection (particularly after bone marrow transplant or in the setting of febrile neutropaenia) 2. Each vial contains 50 mg of amphotericin B, intercalated into a liposomal membrane. Following reconstitution with sterile water for injection, the resulting pH of the suspension is between 5-6. Immediately shake vial vigorously for 30 seconds to completely disperse powder (concentration = 4mg/ml). Add required volume of reconstituted solution using 5-micron filter provided to D5W giving a concentration of 2mg/ml (i. Infuse over 120 minutes (infusion time may be reduced to 60 minutes if the medication is well tolerated) Store refrigerated at 2-8 degrees. Reconstituted solution contains no preservative and should be refrigerated at 2-8 degrees celcius and discarded 24 hours after preparation. Aseptic technique must be strictly observed in all handling since no preservative or bacteriostatic agent is present in AmBisome or in the materials specified for reconstitution and dilution. When this drug is administered for the first time an initial infusion of 10% of the total dose over 30 minutes should be given as a ‘test dose’. If a severe anaphylactic reaction occurs, the infusion should be immediately discontinued and the patient should not receive further infusions of AmBisome. Flucytosine: Concurrent use of flucytosine may increase the toxicity of flucytosine by possibly increasing its cellular uptake and/or impairing its renal excretion. Azoles: In vitro and in vivo animal studies of the combination of amphotericin B and imidazoles suggest that imidazoles may induce fungal resistance to amphotericin B. Combination therapy should be administered with caution, especially in immunocompromised patients. Cardiovascular System: Chest pain, Hypertension, Hypotension, Tachycardia Amphotericin! Drug/Laboratory Test Interactions Salicylates can produce changes in thyroid function tests. Digestive System: Dyspepsia, thirst, nausea, vomiting, diarrhoea, acute reversible hepatotoxicity, gastrointestinal bleeding, and/or ulceration. Nervous System: Mental confusion, drowsiness, and dizziness Skin: Urticaria, angioedema, and pruritus. Haematological System: Prolongation of bleeding time, leukopaenia, thrombocytopaenia, purpura, decreased plasma iron concentration and shortened erythrocyte survival time. Special Senses: Tinnitus, vertigo, reversible hearing loss, and dimness of vision. This preferential effect is not absolute, however, and at higher doses, atenolol inhibits beta2-adrenoreceptors, chiefly located in the bronchial and vascular musculature. Approximately 50% of an oral dose is absorbed from the gastrointestinal tract, the remainder being excreted unchanged in the faeces. Discontinuation of therapy Discontinuation of therapy in a patient with coronary artery disease may lead to rebound angina, arrhythmia or myocardial infarction. Diabetes and Hypoglycaemia Beta blockers may mask tachycardia occurring with hypoglycaemia. Atorvastatin is rapidly absorbed after oral administration; maximum plasma concentrations occur within 1-2 hours. Skeletal Muscle Rare cases of rhabdomyolysis with acute renal failure secondary to myoglobinuria have been reported with atorvastatin and with other drugs in this class. Atracurium besylate slowly loses potency with time at the rate of approximately 6%/year under refrigeration. Upon removal from refrigeration to room temperature storage conditions, use atracurium besylate within 14 days even if re-refrigerated. Special caution should be exercised in administering atracurium besylate to patients in whom substantial histamine release would be especially! The use of a peripheral nerve stimulator is especially important for assessing neuromuscular block in these patients. When there is a need for long-term mechanical ventilation, the benefits-to-risk ratio of neuromuscular block must be considered. Laudanosine, a major biologically active metabolite of atracurium without neuromuscular blocking activity, produces transient hypotension and, in higher doses, cerebral excitatory effects (generalized muscle twitching and seizures) when administered to several species of animals. The prior administration of succinylcholine does not enhance the duration, but quickens the onset and may increase the depth, of neuromuscular block induced by atracurium besylate. More precisely, however, it is termed an antimuscarinic agent since it antagonizes the muscarine-like actions of acetylcholine and other choline esters. Conventional systemic doses may precipitate acute glaucoma in susceptible patients, convert partial organic pyloric stenosis into complete obstruction, lead to complete urinary retention in patients with prostatic hypertrophy or cause inspissation of bronchial secretions and formation of dangerous viscid plugs in patients with chronic lung disease. Leukopaenia and thrombocytopaenia: Severe leukopaenia and/or thrombocytopaenia may occur in patients on azathioprine.

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Internet Content-control software is a form of software designed for controlling what content is permitted to a user on the internet buy discount zudena 100 mg on-line. The restrictions on which web pages can be accessed can be applied at various levels buy zudena 100mg low price. While research has not investigated the impact of these forms of software on reducing illicit drug use discount zudena 100 mg, they may represent useful tools in restricting exposure of drug influences to young people order 100mg zudena with visa. British Medical Association (2006) Legalising illicit drugs: a signposting resource. Ministry of Health (1926) Report of the Departmental Committee on Morphine and Heroin Addiction (The Rolleston Report). World Health Organization (2007) International statistical classification of diseases and related health problems, 10th revision (2e). American Psychiatric Association (1994) Diagnostic and statistical manual of mental disorders (4e). Goldman D, Oroszi G & Ducci F (2005) The genetics of addictions: uncovering the genes. House of Commons Science and Technology Select Committee Drug classification: making a hash of it: fifth report of session 2005-2006. European Monitoring Centre for Drugs and Drug Addiction (2011) Annual report on the state of the drugs problem in Europe. Hoare J & Moon D (eds) (2010) Drug misuse declared: findings from the 2009/10 British Crime Survey. Home Office (2012) Drug misuse declared: findings from the 2011/2012 British Crime Survey. The Scottish Government (2012) 2010-11 Scottish crime and justice survey: drug use. Department of Justice (2010) Experience of drug misuse: findings from the 2008/09 Northern Ireland Crime Survey. Hay G, Gannon M, Casey J et al (2011) Estimates of the prevalence of opiate use and/or crack cocaine use, 2009/10: Sweep 6 report. Fuller E (2012) Smoking, drinking and drug use amongst young people in England 2011. Measham F, Moore K, Newcombe R et al (2010) Tweaking, bombing, dabbing and stockpiling: the emergence of mephedrone and the perversity of prohibition. Newcombe R (2004) Attitudes to drug policy and drug laws: a review of the international evidence. Royal Society for the encouragement of Arts, Manufactures and Commerce (2007) Drugs – facing facts. Bailey R, Fuller E & Ormston R (2010) Smoking, drinking and drugs: reaction to reform. Scottish Government (2010) Scottisocial attitudes survey 2009: public attitudes to drugs and drug use in Scotland. Roques B (1999) La dangerosité de drogues: rapport au Secrétariat d’Etat à la Santé. Best D, Gross S, Vingoe L et al (2003) Dangerousness of drugs: a guide to the risks and harms associated witubstance use. Rolles S & Measham F (2011) Questioning the method and utility of ranking drug harms in drug policy. Nutt D (2011) Let not the best be the enemy of the good: a reply to Caulkins et al. Room R (2011) Scales and blinkers, motes and beams: whose view is obstructed on drug scheduling? Darke S & Hall W (2003) Heroin overdose: research and evidence-based intervention. Darke S, Degenhardt L & Mattik R (2007) Mortality amongst illicit drug users: epidemiology, causes and intervention. O’Driscoll P, McGough J, Hogan H et al (2001) Predictors of accidental fatal drug overdose among a cohort of injection drug users. Warner-Smith M, Darke S, Lynskey M et al (2001) Heroin overdose: causes and consequences. Favrod-Coune T & Broers B (2010) The health effect of psychostimulants: a literature review. Singleton J, Degenhardt L, Hall W et al (2009) Mortality among amphetamine users: a systematic review of cohort studies. Srisurapanont M, Ali R, Marsden J et al (2003) Psychotic symptoms in methamphetamine psychotic in- patients. Aldington S, Harwood M, Cox B et al (2008) Cannabis use and risk of lung cancer: a case-control study. Hall W (2009) The adverse health effects of cannabis use: what are they, and what are their implications for policy? Kuepper R, Van Os J, Lieb R et al (2011) Continued cannabis use and risk of incidence and persistence of psychotic symptoms: 10 year follow-up cohort study. Advisory Council on the Misuse of Drugs (2008) Cannabis: classification and public health. Arseneault L, Cannon M, Witton J et al (2004) Causal association between cannabis and psychosis: examination of the evidence. Rubino T, Zamberletti E & Parolaro D (2012) Adolescent exposure to cannabis as a risk factor for psychiatric disorders. Macleod J, Oakes R, Copello A et al (2004) Psychological and social sequelae of cannabis and other illicit drug use by young people: a systematic review of longitudinal, general population studies. A scientific statement from the American Heart Association Acute Cardiac Care Committee of the Council on Clinical Cardiology. Darke S, Kaye S & Duflou J (2006) Comparative cardiac pathology among deaths due to cocaine toxicity, opioid toxicity and non-drug-related causes. Kaye S & Darke S (2004) Non-fatal cocaine overdose among injecting and non-injecting cocaine users in Sydney, Australia. Alaraj A, Wallace A, Mander N et al (2010) Effect of acute cocaine use on vasospasm and outcome in aneurysmal subarachnoid hemorrhage. Kaye S & Darke S (2004) Injecting and non-injecting cocaine use in Sydney, Australia: physical and psychological morbidity. European Monitoring Centre for Drugs and Drug Addiction (2007) Cocaine and crack cocaine: a growing public health issue. Darke S, Kaye S & Duflou J (2005) Cocaine related fatalities in New South Wales, Australia 1993-2002. Rogers G, Elston J, Garside R et al (2009) The harmful health effects of recreational ecstasy: a systematic review of observational evidence. Miotto K, Darakjian J, Basch J et al (2001) Gamma-hydroxybutyric acid: patterns of use, effects and withdrawal. Hickman M, Carnwath Z, Madden P et al (2003) Drug-related mortality and fatal overdose risk: pilot cohort study of heroin users recruited from specialist drug treatment sites in London. Smyth B, Hoffman V, Fan J et al (2007) Years of potential life lost among heroin addicts 33 years after treatment. Shahani R, Streutker C, Dickson B et al (2007) Ketamine-associated ulcerative cystitis: a new clinical entity.

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