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The form requests information on you symptoms nicotine withdrawal avandia 2 mg free shipping, your supervisor and assessors as well as your thesis title and abstract medicine 5513 purchase avandia 4 mg on line. D Continuation Report Research Presentation Day at School of Medicine event arranged by the Director of Teaching & Learning Postgraduate A Continuation Interview to discuss results and progress arranged by the Supervisor medicine vicodin cheap avandia american express. D Continuation assessors will usually be from within the School of Medicine medications available in mexico cost of avandia, and will have the appropriate expertise to evaluate the submitted work. These procedures are compatible with broad guidelines in the College Calendar, Part 2 Section 2. D Register Arrange a Continuation Interview, on the same day or close to the presentation session. Submit a Progress Report to your assessors Any scientific papers published or in-press, for which the student is first author, may be used as a basis for the Continuation Report. This course of action should be discussed with the Director of Postgraduate Teaching and Learning prior to submission. The following applies (please also see note [2] below): use a font of your choosing font size should be 10-point size text should be single spaced pages must be numbered figures should clear and with own figure legends you may choose any bibliographic style, but be consistent, bibliography should be in font size 8-point size the continuation report will be shorter than a completed thesis but should have the same headings as described below (please see General Thesis Structure). In addition, the Continuation report following should have the following two sections: Future Directions ­ Describe the approaches and experiments that are yet to be undertaken. Thesis plan ­ Finally, present a chapter-by-chapter outline of how you envisage your thesis. The thesis plan could be up to two pages in length, and will describe chapters that are complete, on-going and planned. Ask yourself also if the size of figures can be reduced without compromising clarity, or presentation. The process will consist of a short presentation (10-15 min) with time for questions and discussion. Dependent on your presentation style you may have 10-17 slides (this is not a prescriptive, but purely a guide). The first slide should contain the title, your name and the name(s) of the supervisors(s). The purpose of the talk is to aid your assessors, so your talk should comprise of an introductio, a summary of the research questions/hypotheses, a description of the findings to date, a discussion of these findings and a plan for the future. Research aims, questions and hypotheses: You should have a slide that summarises your aims, hypotheses or questions. Description of the findings: How you answered these questions or sought to prove the hypotheses will be described in the bulk of the presentation. You need not present every single piece of data you have generated in the past 18 months. Discussion: In these slides you will discuss the importance of your data, how it relates to the field, and how has it advanced our understanding. You might also talk about experimental approaches that may have not worked, and how you might trouble shoot these experiments. Plan for the future: A key question for the continuation panel is how the research will continue and become worthy of a higher degree. Essentially you can describe what experiments you will do and how long will these will take. You might even consider grouping your research into areas that could form the basis of thesis chapters. Also in these slides, you might allude to papers (planned, submitted, accepted etc) or conferences you have attended or will attend. Acknowledgements: Thank those who assisted and facilitated you, including, co-workers, collaborators, funders and supervisors. The interview is scheduled and arranged by the Supervisor or a person nominated by the Head of Discipline. Where possible the interview should be arranged on the same day or close to the presentation session. Based on their assessment of the quality of the Continuation Report and the ability of the student to present and discuss their results, the Ph.

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Further Information Talk to your doctor or pharmacist Visit the National Asthma Council Australia website at: nationalasthma medicine urinary tract infection generic avandia 2 mg free shipping. The National Asthma Council Australia expressly disclaims all responsibility (including negligence) for any loss medicine you can give dogs cheap 4 mg avandia, damage or personal injury resulting from reliance on the information contained medicine while breastfeeding order avandia 4 mg without prescription. Acknowledgements Developed by the National Asthma Council Australia in consultation with an expert panel of clinicians with a special interest in complementary therapies and asthma symptoms mononucleosis purchase cheap avandia on line. Supported through funding from the Australian Government Department of Health and Ageing. To access more brochures in this series, visit the National Asthma Council Australia: nationalasthma. Quality asthma care involves not only initial diagnosis and treatment to achieve asthma control, but also long-term, regular follow-up care to maintain control. Asthma control focuses on two domains: (1) reducing impairment-the frequency and intensity of symptoms and functional limitations currently or recently experienced by a patient; and (2) reducing risk-the likelihood of future asthma attacks, progressive decline in lung function (or, for children, reduced lung growth), or medication side effects. Achieving and maintaining asthma control requires providing appropriate medication, addressing environmental factors that cause worsening symptoms, helping patients learn selfmanagement skills, and monitoring over the long term to assess control and adjust therapy accordingly. The diagram (right) illustrates the steps involved in providing quality asthma care. Medications and dosages were updated in September 2011 for the purposes of this quick reference guide to reflect currently available asthma medications. Determine that symptoms of recurrent airway obstruction are present, based on history and exam. Assess at each visit: asthma control, proper medication technique, written asthma action plan, patient adherence, patient concerns. Obtain lung function measures by spirometry at least every 1­2 years; more frequently for asthma that is not well controlled. Determine if therapy should be adjusted: Maintain treatment; step up, if needed; step down, if possible. Teach and reinforce at each visit: Self-monitoring to assess level of asthma control and recognize signs of worsening asthma (either symptom or peak flow monitoring) Taking medication correctly (inhaler technique, use of devices, understanding difference between long-term control and quick-relief medications) - Long-term control medications (such as inhaled corticosteroids, which reduce inflammation) prevent symptoms. If used >2 days/week (except as needed for exercise-induced asthma), the patient may need to start or increase long-term control medications. Teach patients how to use the asthma action plan to: Take daily actions to control asthma Adjust medications in response to worsening asthma Seek medical care as appropriate Encourage adherence to the asthma action plan. Control of Environmental Factors and Comorbid Conditions Recommend ways to control exposures to allergens, irritants, and pollutants that make asthma worse. Consider allergic bronchopulmonary aspergillosis, gastroesophageal reflux, obesity, obstructive sleep apnea, rhinitis and sinusitis, and stress or depression. Treating asthma with medications is safer for the mother and fetus than having poorly controlled asthma. Seek medical care if there is serious deterioration or lack of response to treatment. Urgent or Emergency Care Assess severity by lung function measures (for ages 5 years), physical examination, and signs and symptoms. Consider adjunctive treatments, such as intravenous magnesium sulfate or heliox, in severe exacerbations unresponsive to treatment. Monitor response with repeat assessment of lung function measures, physical examination, and signs and symptoms, and, in emergency department, pulse oximetry. Recommendations for initiating therapy based on level of severity are presented in the last row. Risk Asthma exacerbations requiring oral systemic corticosteroids 0­1/year 2/year 2 exacerb. Frequency and severity may fluctuate over time for patients in any severity category. Step 4 or 5 the stepwise approach is meant to help, not replace, the clinical decisionmaking needed to meet individual patient needs. In 2­6 weeks, depending on severity, assess level of asthma control achieved and adjust therapy as needed.

Urinary tract infections Women: 500 mg orally every 8 hours for 5 days (for uncomplicated infections) symptoms of buy cheap avandia on-line. Localized purulent skin lesions and impetigo Adults: 500 mg orally every 6 hours for 5­7 days medicine youkai watch buy avandia 4 mg amex. Cellulitis and erysipelas Adults: 500 mg orally every 6 hours to complete the treatment course of 7­10 days treatment quadriceps pain cost of avandia, following initial therapy with cefazolin 1­2 g i symptoms low potassium cheap avandia 2 mg with amex. Pyomyositis Adults: 500 mg orally every 6 hours to complete the treatment course of 5­10 days, following initial therapy with cefazolin 1­2 g i. Osteomyelitis due to Staphylococcus aureus in adults and children > 5 years Adults: 1­2 g orally every 6 hours to complete the treatment course of 4­6 weeks, following initial therapy with cefazolin 1­2 g i. Children > 5 years: 25 mg/kg (maximum 500 mg) orally every 6 hours to complete the treatment course of 3­4 weeks, following initial therapy with either ceftriaxone 50­75 mg/kg (maximum 1 g) i. Septic arthritis due to Staphylococcus aureus in adults and children > 5 years Adults: 1­2 g orally every 6 hours to complete the treatment course of 2­3 weeks, following initial therapy with cefazolin 1­2 g i. Children > 5 years: 25 mg/kg (maximum 500 mg) orally every 6 hours to complete the treatment course of 2­3 weeks, following initial therapy with either ceftriaxone 50­75 mg/kg (maximum 1 g) i. In some cases, especially in adults, repeated aspiration or surgical washout of the joint may be necessary. Skin rashes are relatively frequent, while urticaria, bronchospasm and anaphylaxis are uncommon. Cefazolin Powder for injection, 500 mg in vial General information Cefazolin is a first-generation cefalosporin that is active against many Grampositive aerobic cocci but has limited activity against Gram-negative bacteria. It is poorly absorbed from the gastrointestinal tract and must be administered parenterally. Dosage and administration Pneumonia due to Staphylococcus aureus in adults and children > 5 years Adults: 1­2 g i. Osteomyelitis due to Staphylococcus aureus in adults and children > 5 years Adults: 1­2 g i. Septic arthritis due to Staphylococcus aureus in adults and children > 5 years Adults: 1­2 g i. Initial empirical therapy for septicaemia in adults and children > 5 years 1­2 g i. It is bactericidal against Gram-negative organisms, including Pseudomonas aeruginosa, and certain Gram-positive bacteria. Dosage and administration Severe croup (laryngotracheobronchitis) in neonates 50 mg/kg i. Osteomyelitis due to Haemophilus influenzae or unknown pathogen in neonates 50­75 mg/kg (maximum 2 g) i. Clinical information Uses Treatment of: severe croup (laryngotracheobronchitis) in neonates epiglottitis in neonates, together with rifampicin neonatal pneumonia osteomyelitis due to Haemophilus influenzae or unknown pathogen in neonates, together with cloxacillin and amoxicillin + clavulanic acid osteomyelitis due to Salmonella spp. Initial empirical therapy for septic arthritis in neonates 50­75 mg/kg (maximum 2 g) i. Septic arthritis due to Staphylococcus aureus in neonates 50­75 mg/kg (maximum 2 g) i. Initial empirical therapy for septicaemia in neonates 50­75 mg/kg (maximum 2 g) i. Rarely, antimicrobial-associated pseudomembranous colitis due to Clostridium difficile occurs. After intramuscular administration, the drug is widely distributed throughout the body and is excreted primarily unchanged in the urine. After the initial intensive therapy, eradication of any secondary infection is recommended with oral sulfamethoxazole + trimethoprim or doxycycline for at least 3 months. Clinical information Uses Treatment of: nosocomial pneumonia, together with gentamicin or ciprofloxacin melioidosis, together with sulfamethoxazole + trimethoprim or doxycycline. Skin rashes are relatively frequent, while urticaria, bronchospasm and anaphylaxis are 112 Drugs uncommon. Ceftriaxone Powder for injection, 250 mg (as sodium salt) in vial General information Ceftriaxone is a third-generation cefalosporin derived from Cephalosporium acremonium. After intramuscular administration, ceftriaxone is distributed widely throughout the body. It has a relatively long plasma half-life of about 8 hours and is excreted unchanged in both urine and bile. Very severe pneumonia in children aged from 2 months to 5 years 50 mg/kg (maximum 1 g) i.

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Endogenous ligands have sometimes been discovered long after the drugs that act on their receptors 3 medications that affect urinary elimination generic avandia 4mg mastercard. Endorphins and enkephalins (endogenous ligands of morphine receptors) were discovered many years after morphine medications you can take when pregnant buy avandia 4 mg online. Control concentration/dose­response curves for an agonist A together with curves in the presence of (a) a competitive antagonist B and (b) a non-competitive antagonist C treatment zamrud purchase avandia 2 mg without prescription. Increasing concentrations of the competitive antagonist ([B]1 medications januvia buy cheap avandia 2 mg line, [B]2) cause a parallel shift to the right of the log dose­effect curve (a), while the non-competitive antagonist ([C]1, [C]2) flattens the curve and reduces its maximum (b). Provided that the dose of agonist is increased sufficiently, a maximal effect can still be obtained, i. If a dose (C) of agonist causes a defined effect when administered alone, then the dose (C) needed to produce the same effect in the presence of antagonist is a multiple (C /C) known as the dose ratio (r). This results in the familiar parallel shift to the right of the log dose­response curve, since the addition of a constant length on a logarithmic scale corresponds to multiplication by a constant factor (Figure 2. By contrast, antagonists that do not combine with the same receptor (non-competitive antagonists) or drugs that combine irreversibly with their receptors, reduce the slope of the log dose­response curve and depress its maximum (Figure 2. Physiological antagonism describes the situation where two drugs have opposing effects. The potency of the antagonist (pA2) is determined from the intercept of the Schildt plot. Such measurements provided the means of classifying and subdividing receptors in terms of the relative potencies of different antagonists. Second, it is more difficult to reverse the effects of a partial agonist, such as buprenorphine, with a competitive antagonist such as naloxone, than it is to reverse the effects of a full agonist such as morphine. A larger fraction of the receptors is occupied by buprenorphine than by morphine, and a much higher concentration of naloxone is required to compete successfully and displace buprenorphine from the receptors. Alternatively, G-proteinmediated linkage between receptors and effector enzymes. Since G-proteins link several distinct receptors to the same effector molecule, this can give rise to heterologous desensitization. Desensitization is probably involved in the tolerance that occurs during prolonged administration of drugs, such as morphine or benzodiazepines (see Chapters 18 and 25). Gonadotrophin-releasing hormone is released physiologically in a pulsatile manner. Several partial agonists are used in therapeutics, including buprenorphine (a partial agonist at morphine -receptors, Chapter 25) and oxprenolol (partial agonist at -adrenoceptors). One example of clinical importance is increased -adrenoceptor numbers following prolonged use of beta-blockers. Abrupt drug withdrawal can lead to tachycardia and worsening angina in patients who are being treated for ischaemic heart disease. Case history A young man is brought unconscious into the Accident and Emergency Department. He is unresponsive, hypoventilating, has needle tracks on his arms and pinpoint pupils. Naloxone is administered intravenously and within 30 seconds the patient is fully awake and breathing normally. He is extremely abusive and leaves hospital having attempted to assault the doctor. Comment the clinical picture is of opioid overdose, and this was confirmed by the response to naloxone, a competitive antagonist of opioids at -receptors (Chapter 25). It would have been wise to have restrained the patient before administering naloxone, which can precipitate withdrawal symptoms. He will probably become comatose again shortly after discharging himself, as naloxone has a much shorter elimination half-life than opioids such as morphine or diacetyl-morphine (heroin), so the agonist effect of the overdose will be reasserted as the concentration of the opiate antagonist falls. Examples include antacids (which neutralize gastric acid), osmotic diuretics (which increase the osmolality of renal tubular fluid), and bulk and lubricating laxatives. Oxygen is an example of a highly specific therapeutic agent that is used in high concentrations (Chapter 33). Metal chelating agents, used for example in the treatment of poisoning with ferrous sulphate, are examples of drugs that exert their effects through interaction with small molecular species rather than with macromolecules, yet which possess significant specificity. General anaesthetics (Chapter 24) have low molar potencies determined by their oil/water partition coefficients, and low specificity. Key points Most drugs are potent and specific; they combine with receptors for endogenous mediators or with high affinity sites on enzymes or other proteins.

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Fibroblasts and macrophages are the most common cells in loose connective tissue medicine used to treat chlamydia avandia 2mg amex, but mast cells medicine during pregnancy order avandia in united states online, plasma cells treatment plan goals purchase avandia with american express, neutrophils and fat cells may also be found treatment diarrhea 2 mg avandia. Examine the scanned image at low power, and note that one surface is indented by pits that are lined by columnar epithelial cells. Immediately beneath these cells is the loose connective tissue called lamina propria. These fibers (type I collagen) are colored red-brown by the counterstain Azo-carmine. The black, silver-stained reticular fibers form the supporting framework for the cortical nodules. The lymphocytes, which are located within the interstices of this framework, are not well seen in this slide. The epithelium (epidermis) and dense, irregularly arranged connective tissue appear deeply stained. At higher magnification observe that the intracytoplasmic lipid has been extracted from the fat cells during the histological preparation of the tissue. The thin peripheral ring of cytoplasm and the flattened peripheral nucleus, coupled with the large central vacuole results in the "signet ring" appearance of fat cells. At higher magnification observe the white fat in which each cell contains a single fat droplet (unilocular). In brown fat cells the lipid is accumulated in droplets, giving the cells a multilocular appearance. Its thick collagenous (type I) bundles stain intensely with eosin and can be seen to course in various directions. Immediately surrounding the lining cells is a very small zone of pale-staining loose areolar connective tissue. Outside of this, there is a large zone of acidophilic dense irregularly arranged connective tissue. Clumps of white adipose tissue are scattered throughout the stroma of the mammary gland. Rows of fibroblasts with heterochromatic nuclei are aligned between the collagenous bundles. Compare the appearance of the collagen bundles (Type I collagen) and fibroblasts with that of the skeletal muscle fibers on the same section. Collagen is stained pink and can be distinguished from skeletal muscle that is stained purple. Elastic fibers stain reddish-brown to black and form prominent fenestrated, elastic sheets in the aorta. Understand the differences between the development and growth of cartilage and bone. Describe the processes of intramembranous bone development and endochondral ossification. As in other connective tissues, its matrix is composed of fibers (collagenous or elastic) and a ground substance that is rich in extracellular glycosaminoglycans (particularly the chondroitin sulfates). Cartilage is avascular, but its matrix is permeable to nutrients and waste products. Cartilage is the primary skeletal tissue of the fetus, and it serves as a model for the development of endochondral bone. In the adult, cartilage forms the articular surfaces of joints, the skeleton of the external ear, the septum of the nose, supporting rings and plates of the trachea and bronchi, and intervertebral discs. Three types of cartilage are found in the adult: hyaline, elastic, and fibrocartilage. These are classified according to the predominant component of their extracellular matrix. As in other connective tissue classifications, there are gradations between these basic types. At higher magnification observe that a perichondrium surrounds the cartilage; this merges with the cartilage on one side and with the surrounding connective tissue of the other side. Blood vessels within the perichondrium provide the blood supply for the avascular cartilage. Chondroblasts are cells adjacent to the perichondrium and recently derived from it.

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