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Primary Expression (primary + expression)
Selected AbstractsAtypical attack of acute intermittent porphyria , paresis but no abdominal painJOURNAL OF INTERNAL MEDICINE, Issue 3 2002C. Andersson Abstract.,Andersson C, Nilsson A, Bäckström T (University Hospital, Umeå, Sweden; and Primary Health Care Centre, Arvidsjaur). Atypical attack of acute intermittent porphyria , paresis but no abdominal pain (Case report). J Intern Med 2002; 252: 265,270. We report a case of acute intermittent porphyria (AIP) in a 45-year-old woman. Her first attack occurred at the age of 38. Because of escalating cyclical premenstrual attacks, the following 2 years, depletion of the endogenous sex hormone was considered as haeme arginate treatment proved insufficient. Gonadotropin releasing hormone agonist treatment with low-dose oestradiol add back was quite successful initially but was abandoned after 18 months when progesterone add back precipitated a severe attack. Following hysterectomy and oophorectomy at age 42 and oestradiol add back, a remarkable monthly regularity of attacks ensured periodically but with milder symptoms. Two years after surgery, preceded by six attack-free months, a puzzling symptom-shift occurred, from abdominal pain, back and thigh pain during the attacks, to solely severe distal extensor paresis in the arms. Haeme arginate treatment interrupted the progress of the paresis almost immediately and motor function improved considerably up to the 9-month follow-up. Electrophysiological examination revealed only motor neuropathy, consistent with axonal degeneration. Subsequently the symptoms changed yet again, to sensory disturbances with numbness and dysesthesia as the primary expression followed by rather mild abdominal pain. However, cyclical attacks occurred, despite absence of endogenous ovarial hormone production, possibly attributable to impaired oestrogen metabolism in the liver, or adrenal oestrogen production. Treatment comprising oophorectomy, low-dose oestradiol add back and haeme arginate infusion for 2 days on the appearance of early AIP symptoms is now quite successful affording improvement in life quality. [source] Review: low caloric intake and gall-bladder motor functionALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2000D. Festi Summary Cholelithiasis is the primary expression of obesity in the hepatobiliary system. In obese subjects the risk of developing gallstones is increased due to a higher cholesterol saturation of gall-bladder bile. During weight reduction with very low calorie diets (VLCD) the incidence of gallstones increases, but the mechanism for gallstone formation is not completely understood and several pathogenetic mechanisms have been suggested: increased saturation of bile, increased gall-bladder secretion of mucin and calcium, increased presence of prostaglandins and arachidonic acid. Alterations in gall-bladder motility may contribute to gallstone formation, but few studies have addressed the issue of gall-bladder motility during rapid weight loss and its possible role in gallstone formation. VLCD have been associated with a gall-bladder stasis, as a consequence of reduced gall-bladder stimulation by low fat content of the diets. A threshold quantity of fat (10 g) has been documented to obtain efficient gall-bladder emptying. Ursodeoxycholic acid administered during VLCD seems to have a protective role in developing a biliary cholesterol crystals. Gall-bladder emptying was lower in response to low fat meals with respect to relative higher fat meals, before as well as during the VLCD. This may account the possibility of an adaptative response of the gall-bladder motility to a given diet regimen. Adequate fat content of the VLCD may prevent gallstone formation, maintaining adequate gall-bladder motility and may be more economic and physiologically acceptable than administration of a pharmacological agent. [source] Talk About Terrorism and the Media: Communicating With the Conduit MetaphorCOMMUNICATION, CULTURE & CRITIQUE, Issue 4 2008Simon J. Harrison The conduit metaphor is the primary expression of linguistic communication in our culture (M. J. Reddy, 1979). It structures theories and frameworks based on the "Code Model" (from C. E. Shannon & W. Weaver, 1949) such as the Social Amplification of Risk Framework (R. E. Kasperson et al., 1988; N. Pidgeon, R. E. Kasperson, & P. Slovic, [Eds] 2003). The conduit metaphor structure objectifies source, receiver, and messages, which are talked of as "objects" or "substances" passed along a conduit to a receiver to be recovered. Metaphor analysis of 6 semistructured interviews with laypersons about terrorism and the media showed how the conduit metaphor structures a subjective process of reification, quantification, comparison, and judgment. This interpretation suggests that the demands of the conduit metaphor structure for the transferred message to be "invariant" and "pure" can influence relationships of trust and blame between media and public. The authors suggest that a notion of interactive communication between the media and the public should take into consideration the power of the conduit metaphor structure to shape understandings. [source] Saying and Showing: Art, Literature and Religious UnderstandingMODERN THEOLOGY, Issue 1 2002Patrick J. Sherry I argue that works of art and literature can be primary expressions of religious ideas, i.e., ones not dependent on other modes of communication like preaching or theology. This does not mean, however, that such works are independent of criticism, for an artist or writer can show something that is untrue, immoral, crude, and so on. I maintain that art and literature may criticize theology, or vice versa; or, thirdly, the relationship between them may be reciprocal, and I illustrate these three possibilities via Ibsen's Brand, Goethe's Faust, and the film Dead Man Walking. [source] | |||||||||||||