By Q. Mazin. University of Saint Mary. 2018.
The vexed question of authorship: view of researchers in a British medical faculty discount 100mg trandate with amex blood pressure medication urination. Broad-spectrum antibiotics for preterm discount trandate 100mg free shipping blood pressure chart age 50, prelabour rupture of fetal membranes: the ORACLE I randomised trial. In Vancouver format, the author list must have surnames followed by initials with no full stops and separated by commas. When citing a reference, the first six authors are listed followed by et al. The National Library of Medicine (www3) lists up to 24 authors before et al. The title is followed by a full stop, one space, the journal name abbreviated using Index Medicus guidelines, one space, the year of publication, a semicolon, the volume, a colon and then the page numbers followed by a full stop. Abbreviated journal names are published each year in the January issue of Index Medicus or can be found at the website (www2). If you are unsure of the correct abbreviation to use, quote the journal name in full since it is not acceptable to make up your own abbreviation. The use of an electronic reference management database (www9) is an essential tool for any writer. Because most reference manager programs will readily produce reference lists in a variety of styles and formats, it is prudent to invest in using this type of software. In this way, the reference needs only to be entered once, perhaps by downloading from a bibliographic database such as MEDLINE® or PubMed®. You can then add and delete references or reorganise the text in your paper in the knowledge that your software will renumber your references correctly in the final version. You should never use phrases in your paper or enter citations into your database that you have copied from another paper. Even public databases may have some errors, so always be 103 Scientific Writing thorough and obtain a copy of the original article so that you can check that your electronic references are absolutely correct. It is essential to ensure that the article says what other people say it says and check its exact citation details. You can then cite any article liberally in the knowledge that the reference is always correct. Errors in the year of publication, the volume number or the page numbers make it very difficult and very frustrating for fellow researchers who want to retrieve the cited article. High error rates that have been identified in citations, mostly in authors’ names and the title,25 are both unacceptable and easily preventable. As an author, you are entirely responsible for the accuracy of your references, the details of which will not be checked by the journal or copy editors. Errors in references detract from the quality of your paper and suggest that you may also have lacked attention to detail in collecting and reporting the data. Moreover, quoting second-hand sets up chains of Chinese whispers that perpetuate errors as they are transcribed from one author to the next. As such, these compounding errors will detract from your scientific reputation because your mistake will become public when the Scientific Citation Index (see Chapter 6) records your incorrect citations and helps to pinpoint their origin. When you are writing your paper, always quote the science and not the scientist. When you cite the work of other researchers, you need to compare your results with their results or say what they found. If you use some researchers’ names and not others, you tend to add a name dropping importance to selective work. Also, the practice ignores the contributions of the coauthors whose names are omitted. It is best not to use names at all but, if you really do want to, then you should use them consistently for all citations throughout. If you really want to cite another research group by name, be convinced that you really need to do this and only cite the head of the research group. That said, on rare occasions it may be important to highlight the work of another group of scientists, for example when you are writing rebuttals to comments made by the reviewers of a grant application.
This may explain generic trandate 100 mg overnight delivery prehypertension at 25, in part discount 100mg trandate with visa blood pressure log sheet, why more females than males suffer from most kinds of chronic pain as well as painful autoimmune diseases such as multiple sclerosis and lupus. Some forms of chronic pain may occur as a result of the cumulative de- structive effect of cortisol on muscle, bone, and neural tissue. Furthermore, loss of fibers in the hippocampus due to aging reduces a natural brake on cortisol release that is normally exerted by the hippocampus. As a result, cortisol is released in larger amounts, producing a greater loss of hippo- campal fibers and a cascading deleterious effect. It could explain the increase of chronic pain problems among older people. The cortisol output by itself may not be sufficient to cause any of these problems, but rather provides the conditions so that other contributing fac- tors may, all together, produce them. Sex-related hormones, genetic predis- positions, psychological stresses derived from social competition, and the hassles of everyday life may act together to influence cortisol release, its amount and pattern, and the effects of the target organs. Chrousos and Gold (1992) documented the effects of dysregulation of the cortisol system: effects on muscle and bone, to which they attribute fibromyalgia, rheuma- toid arthritis, and chronic fatigue syndrome. They proposed that they are caused by hypocortisolism, which could be due do depletion of cortisol as 1. Indeed, Sapolsky (1994) attributed myopathy, bone decalcification, fatigue, and accelerated neural degeneration during aging to prolonged exposure to stress. Clearly, consideration of the relationship between stress-system effects and chronic pain leads directly to examination of the effects of suppression of the immune system and the development of autoimmune effects. The fact that several autoimmune diseases are also classified as chronic pain syndromes—such as Crohn’s disease, multiple sclerosis, rheumatoid arthri- tis, scleroderma, and lupus—suggests that the study of these syndromes in relation to stress effects and chronic pain could be fruitful. Immune sup- pression, which involves prolonging the presence of dead tissue, invading bacteria and viruses, could produce a greater output of cytokines, with a consequent increase in cortisol and its destructive effects. Furthermore, prolonged immune suppression may diminish gradually and give way to a rebound, excessive immune response. The immune system’s attack on its own body’s tissues may produce autoimmune diseases that are also chronic pain syndromes. Thorough investigation may provide valuable clues for understanding at least some of the terrible chronic pain syn- dromes that now perplex us and are beyond our control. PAIN AND NEUROPLASTICITY There was no place in the specificity concept of the nervous system for “plasticity,” in which neuronal and synaptic functions are capable of being molded or shaped so that they influence subsequent perceptual experi- ences. Plasticity related to pain represents persistent functional changes, or “somatic memories,” (Katz & Melzack, 1990), produced in the nervous system by injuries or other pathological events. The recognition that such changes can occur is essential to understanding the chronic pain syn- dromes, such as low back pain and phantom limb pain, that persist and of- ten destroy the lives of the people who suffer them. Denervation Hypersensitivity and Neuronal Hyperactivity Sensory disturbances associated with nerve injury have been closely linked to alterations in CNS function. Markus, Pomeranz, and Krushelnycky (1984) demonstrated that the development of hypersensitivity in a rat’s hindpaw following sciatic nerve section occurs concurrently with the expansion of the saphenous nerve’s somatotopic projection in the spinal cord. Nerve injury may also lead to the development of increased neuronal activity at every level of the somatosensory system (see review by Coderre, Katz, 30 MELZACK AND KATZ Vaccarino, & Melzack, 1993). In addition to spontaneous activity generated from the neuroma, peripheral neurectomy also leads to increased sponta- neous activity in the dorsal root ganglion and spinal cord. Furthermore, af- ter dorsal rhizotomy, there are increases in spontaneous neural activity in the dorsal horn, the spinal trigeminal nucleus, and the thalamus. Clinical neurosurgery studies reveal a similar relationship between de- nervation and CNS hyperactivity. Neurons in the somatosensory thalamus of patients with neuropathic pain display high spontaneous firing rates, ab- normal bursting activity, and evoked responses to stimulation of body ar- eas that normally do not activate these neurons (Lenz et al. The site of abnormality in thalamic func- tion appears to be somatotopically related to the painful region. In patients with complete spinal cord transection and dysesthesias referred below the level of the break, neuronal hyperactivity was observed in thalamic regions that had lost their normal sensory input, but not in regions with apparently normal afferent input (Lenz et al. Furthermore, in patients with neuropathic pain, electrical stimulation of subthalamic, thalamic, and cap- sular regions may evoke pain and in some instances even reproduce the pa- tient’s pain (Nathan, 1985; Tasker, 1989). Direct electrical stimulation of spontaneously hyperactive cells evokes pain in some but not all pain pa- tients, raising the possibility that in certain patients the observed changes in neuronal activity may contribute to the perception of pain (Lenz, Kwan, Dostrovsky, & Tasker, 1987).
Craigen MAC trandate 100mg discount blood pressure medication online, Watters J 100mg trandate free shipping arteria umbilical, Hackett JS (1992) The changing epidemiol- recurrent multifocal osteomyelitis (CRMO). Stubbs AJ, Gunneson EB, Urbaniak JR (2005) Pediatric femoral akuten infektiösen Osteomyelitis. Beitr Klein Chir 10: 257–65 avascular necrosis after pyarthrosis: use of free vascularized fibu- 10. Girschick HJ, Raab P, Surbaum S, Trusen A, Kirschner S, Schneider lar grafting. Clin Orthop Relat Res 439:193-200 P, Papadopoulos T, Muller-Hermelink HK, Lipsky PE (2005) Chronic 32. Tudisco C, Farsetti P, Gatti S, Ippolito E (1991) Influence of chronic non-bacterial osteomyelitis in children. Ann Rheum Dis 64: 279-85 osteomyelitis on skeletal growth: Analysis at maturity of 26 cases 11. Gordon JE, Wolff A, Luhmann SJ, Ortman MR, Dobbs MB, Schoe- affected during childhood. J Pediatr Orthop 11: 358–63 necker PL (2005) Primary and delayed closure after open irrigation 33. Unkila-Kallio L, Kallio MJ, Peltola L (1994) The usefulness of C- and debridement of septic arthritis in children. J Pediatr Orthop B reactive protein levels in the identification of concurrent septic 14: 101-4 arthritis in children who have acute hematogenous osteomyelitis. A comparison with the usefulness of the erythrocyte sedimenta- In: Weber U, Rettig H, Jungbluth H (ed. Upadhyay SS, Saji MJ, Sell P, Sell B, Hsu LC (1994) Spinal deformity with spinal tuberculosis. A comparison of radiography, computed after childhood surgery for tuberculosis of the spine. A comparison tomography and magnetic resonance imaging J Bone Joint Surg of radical surgery and debridement. Jaberi F, Shahcheraghi G, Ahadzadeh M (2002) Short-term intra- thopäde 26: 902–7 venous antibiotic treatment of acute hematogenous bone and 36. Wang C, Wang S, Yang Y, Tsai C, Liu C (2003) Septic arthritis in joint infection in children: a prospective randomized trial. J Pediatr children: relationship of causative pathogens, complications, and Orthop 22: 317–20 outcome. Warner W, Elias D, Arnold S, Buckingham S, Beaty J, Canale T (2005) 13 years of age – 10 years experience. Injury 34: 776–80 Changing Patterns of Acute Hematogenous Osteomyelitis and 16. Or- Septic Arthritis: Emergence of Community-Acquired Methicillin thopäde 26: 889–93 Resistance. Zimmerli W, Ochsner P (2003) Management of infection associ- North Am 18 (1): 225–46 ated with prosthetic joints. Kahn MF, Hayem F, Hayem G, Grossin M (1994) Is diffuse sclerosing osteomyelitis of the mandible part of the synovitis, acne, pustu- losis, hyperostosis, osteitis (SAPHO) syndrome? Kocher M, Mandiga R, Murphy J, Goldmann D, Harper M, Sundel R, Ecklund K, Kasser J (2003) A clinical practice guideline for treat- ment of septic arthritis in children: efficacy in improving process of care and effect on outcome of septic arthritis of the hip. Lauschke FHM, Frey CT (1994) Hematogenous osteomyelitis in infants and children on the Northwestern region of Namibia. Matzkin EG, Dabbs DN, Fillman RR, Kyono WT, Yandow SM (2005) Chronic osteomyelitis in children: Shriners Hospital Honolulu ex- perience. Mousa HA (1997) Evaluation of sinus-track cultures in chronic bone infection. Children with juvenile rheumatoid arthritis also tend to be rather reserved and seem to have difficulty in expressing their problems and » When a rheumatic child comes for a medical check, conflicts. The joint mucosa Juvenile rheumatoid arthritis is an inflammatory con- becomes edematous and hypervascularized, and an ef- dition that occurs during childhood or adolescence fusion that is moderately rich in leukocytes (particularly and affects one or more joints, although it can also lymphocytes) forms. Over time the synovial cells prolifer- affect other organ systems (particularly the eyes). It ate, causing the synovial membrane to thicken and form tends to affect the major joints rather than the small- nodules and protuberances and, in some cases, cysts. At a er joints of the hands and feet as with the primary later stage fibrinoid degeneration occurs with granuloma- chronic adult form.
Bone scintigraphy is arguably the easiest from abscess cavitation and in determining whether way of searching for other occult or early sites; all the the joints are involved buy trandate 100mg mastercard heart attack aspirin. US is very sensitive and long bones should be included in the examination proven trandate 100mg heart attack xbox. Again the pyogenic organisms Bone scintigraphy used to be the investigation predominate. There is a strong link with penetrating chosen to rule out osteomyelitis when plain films injuries. Muscle infection may be secondary to dif- were normal but it has been supplanted in this fuse soft-tissue cellulitis or to osteomyelitis. There may be rare occasions when MR is also occur spontaneously without other compart- impractical or equivocal when triple-phase bone ments involved, especially in immunosuppressed scintigraphy has a role. MRI is the most useful investigation for staging the extent of disease [29–31] (Fig. The only occasion where infection is likely to be overlooked is when Plain films are sometimes diagnostic with evidence the disease is not yet producing symptoms. Areas of of periosteal reaction and permeative lysis in the oedema (low on T1 and high on T2) are also seen affected areas. Infection typically to sclerosis, new bone formation and even frank leads to adjacent soft-tissue changes but as these are destruction. Unfortunately, in the early stages the common in injuries, this does not help. Plain ﬁlms were normal at this stage b is critical but this may not always be reliable in chil- Biopsies should be taken bearing in mind that the dren or for that matter in adults. The extent of infec- margins may not be representative whilst the centre tion including involvement of joints, abscess forma- of the lesion may be necrotic. It is prudent to take tion and necrosis of the affected bone are all seen on several samples from different areas. The areas infected tend to be sur- at discriminating oedema from a fluid-contain- rounded by oedema and it is not possible to differ- ing abscess; intravenous contrast helps but may be entiate this from truly infected regions. Ultrasound is the best method of show- contrast may increase the ease of discrimination of ing pus or fluid that could be aspirated or removed oedema from infected areas but it is not reliable and and is the ideal means of guiding needle puncture or rarely makes any impact on management decisions. FSTIR MRI shows oedema in the adjacent bone which could be reactive or a sign of early osteomyelitis. Follow-up MR after antibiotic treatment showed resolution of this issue a Fig. Orthopade As detailed above, imaging, especially MRI, is impor- 26(10):830–837 tant in deciding where to biopsy. Robben SG, Meradji M, Diepstraten AF, et al (1998) US of the mass effect seen on MR or detected clinically is the painful hip in childhood: diagnostic value of cartilage an abscess. Most will use fluoroscopy or CT guidance thickening and muscle atrophy in the detection of Perthes’ disease. Radiology 208(1):35–42 to obtain the specimens and US to aspirate fluid. Lee SK, Suh KJ, Kim YW, et al (1999) Septic arthritis versus choice depends on local facilities and individual skills, transient synovitis at MR imaging: preliminary assessment but fluoroscopy is generally faster and less complex with signal intensity alterations in bone marrow. Radiology for bone biopsy and US is more suitable for soft-tissue 211(2):459–465 lesions. Berman L, Fink AM, Wilson D, et al (1995) Technical note: identifying and aspirating hip effusions. Skinner J, Glancy S, Beattie TF, et al (2002) Transient syno- treatment; it is best performed on the same equip- vitis: is there a need to aspirate hip joint effusions? Eur J ment with the same protocols for each follow-up Emerg Med 9(1):15–18 study. Luhmann SJ, Jones A, Schootman M, et al (2004) Differen- tiation between septic arthritis and transient synovitis of is poor at providing images that can be compared the hip in children with clinical prediction algorithms.
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