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My name is Jim Hill and I have been interested in wood carving for many years. In 1990, I took a carving course at Loyalist College. I started by making a Loon in Butternut to learn to develop shape, then did one in Basswood to learn painting techniques. After finishing the courses, I joined the Quinte Wood Carvers in Belleville. With the help of club members, I developed skills to enable me to carve ducks, song birds, stylized human figures, aquatic animals and west coast Indian masks and art. Over the years this hobby has been a stress relief, although it too can be frustrating at times, but when you see the results it is very gratifying. Sometimes we think we do not have the ability to do this, but with some guidance and practice, it is surprising the results you can achieve! In 1995, I joined an informal group called the Cold Creek Carvers. We meet at the Dufferin Centre in Trenton on Wednesdays from September to May. The Quinte Wood Carvers have five general meetings a year and groups presently meet on Thursdays at Moira Secondary School, Belleville and at the Stirling Legion on Saturday mornings, usually September to April. The Quinte Woodturners Guild meet at Club 105 once a month see further details on our `Club Activities' page ; . Wood carving is an activity that can be enjoyed by all age groups and is relatively inexpensive. If you have any questions or would like to know more about this fascinating hobby, please give Jim a call at 394-2187.
On I, . However, in these studies PCP concentrations of 100 or more were used, and at these concentrations we also found that the drug depresses both Z, and IA. In addition to confirming that PCP blocks I, and IA channels with different potencies, the present study also suggeststhat the precise way in which PCP interacts with the 2 channel types may differ. PCP blocks I, channels by binding to a site with a KD of PM. The voltage dependency of the PCP block indicates that the PCP acceptor site senses about 40-50% of the transmembrane electric field. It is likely that the acceptor site is within the channel pore. However, other interpretations of these data are possible. For example, the acceptor site could theoretically be outside the transmembrane electrostatic field if a membrane potential-dependent conformational change altered its binding affinity or it could inhibit ion transit through the channel by binding to an allosteric site within the electrostatic field but outside the pore per se. Block of I, occurs more rapidly than the current activates and does not show use dependency. In addition, ZK channels recover from block even in the absence of voltage-dependent activation unpublished observations ; , indicating that PCP is not trapped within the closed channel. These results suggest that block may occur through a hydrophobic pathway in which the drug is able to bind to closed channels see Hille, 1977 ; . Nevertheless, the possibility cannot be excluded that binding and unbinding are so rapid that neither pseudoinactivation nor use dependency is observed, despite an open channel-blocking mechanism. In contrast to the results with I PCP only weakly blocked I but at high concentrations that caused a substantial reduction in the current there was a marked speeding of the decay rate. In addition, with repeated brief voltage steps, we observed cumulative block of the current which rapidly recovered upon cessation of the drug superfusion. These observations indicate that PCP block of IA is use dependent and suggestthat IA channels must open before they can become blocked, so that block occurs via a hydrophilic pathway. The mechanism by which PCP blocks I, channels may also differ from the way in which PCP-related drugs interact with NMDA receptor channels. As discussed above, there is substantial evidence in favor of the concept that NMDA receptor channels must be in the agonist activated state for binding and block to occur. Moreover, the drug molecule can become trapped within the ionophore when the channels close so that they are only liberated upon reopening MacDonald et al., 1987; Huettner and Bean, 1988 ; . Thus, block ofthe NMDA receptor channel occurs via a hydrophilic mechanism like the block of IA.
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Histological findings in retrieved femoral head remnants following revision of hip resurfacing arthroplasty for early failure * Harding, I; Little, C; Ruiz, A; Murray, D; McLardy-Smith, P; Athanasou, N Correlation between periprosthetic bone loss and stem size after insertion of an uncemented, customized femoral prosthesis * Aamodt, A; Benum, P RGD-peptide surface treatment increases bone ingrowth to press-fit implants. A study in canines * Elmengaard, B; Bechtold, J; Soballe, K Degradation of hydroxyl-apatite HA ; coating around press-fitted porous-coated cups. Scanning electron microscopy study SEM ; * Fadda, M; Zirattu, A; Manunta, A; Fadda, G; Delrio, A N Cemented cup stability after bone impaction grafting is improved when large washed bone chips are used * Arts, J; Schreurs, B W; Verdonschot, N; Buma, P Experience with a novel modular femoral stem for difficult primary and revision hip arthroplasty * Allan, D G; Trammell, R and etodolac.
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Identify the underlying cause as this has important implications for treatment therefore a holistic assessment is vital: l. Medical surgical history - vascular, diabetes, rheumatoid disease, heart failure etc. family history 2. Nutritional status weight 3. Social psychological status - smoking, occupation, depression, housing etc. 4. Clinical investigations - BP, Urinalysis and Doppler ABPI 5. General and ankle mobility 6. Pain - when it occurs and how it is relieved, e.g. arterial ulcer pain increases when leg elevated. 7. Allergies 8. Medication 9. Examination of legs and skin and exemestane.
Whether measured by provider-submitted charges or allowed charges, the high cost incurred by women with endometriosis is due to the high rates of hospital admissions as well as surgical procedures and by the presence of significant comorbid conditions such as infertility, depression, and migraine. Interestingly, when 2004 endometriosis costs are extrapolated from 2003 figures using a 12% trend to account for inflation, the cost of endometriosis rises to 1 PPPM. This is similar or higher to previously and similarly calculated 2004 costs incurred for such high-profile conditions as hypertension 0 ; , diabetes 6 ; , and rheumatoid arthritis , 121 ; and is almost double the average 2004 medical costs for women 5 PMPM ; .41 High rates of endometriosis-related surgery have been previously reported, with one case of a 36-year old woman with a history of 11 surgical procedures related to pelvic pain or endometriosis over 20 years.42 Endometriosis requires histological confirmation, most commonly laparoscopy, for diagnosis. This and other gynecological surgical procedures have the potential for unexpected complications, such as blood loss and transfusion, bladder injury, pulmonary embolism, wound complications, and problems due to general anesthesia.43 The high hospital and surgery rates observed in the current analysis are in line with these findings. In this study, women with endometriosis diagnosis codes had 35 times more hysterectomies and laparotomies and 20 times more oophorectomies compared.
1. Kieffer, T. J. & Habener, J. L. 1999 ; The glucagon-like peptides. Endocr. Rev. 20: 876 913. Burrin, D. G., Stoll, B. & Guan, X. 2003 ; Glucagon-like peptide 2 function in domestic animals. Domest. Anim. Endocrinol. 23: 103122. 3. Drucker, D. J. 2002 ; Gut adaptation and the glucagon-like peptides. Gut 50: 428 435. Drucker, D. J., Ehrlich, P., Asa, S. L. & Brubaker, P. L. 1996 ; Induction of intestinal epithelial proliferation by glucagon-like peptide 2. Proc. Natl. Acad. Sci. 93: 79117916. 5. Dowling, H. 2003 ; GLP-2: An historical perspective. J. Nutr. 133: 37033707. 6. Estall, J. L. & Drucker, D. J. 2003 ; Dual regulation of cell proliferation and survival via activation of GLP-2 receptor signaling. J. Nutr. 133: 3708 3711. Tappenden, K. A. 2003 ; Short-chain fatty acids and GLP-2: A new twist to an old story. J. Nutr. 133: 37173720. 8. Jeppesen, P. B. 2003 ; Clinical significance of GLP-2 in short-bowel syndrome. J. Nutr. 133: 37213724. 9. Burrin, D. G., Stoll, B., Jiang, R., Holst, J. J. & Reeds, P. J. 2000 ; Minimal enteral nutrient requirements for neonatal intestinal growth in piglets: how much is enough? Am. J. Clin. Nutr. 71: 16031610. 10. Xiao, Q., Boushey, R. P., Drucker, D. J. & Brubaker, P. L. 1999 ; Secretion of the intestinotropic hormone glucagon-like peptide 2 is differentially regulated by nutrients in humans. Gastroenterology 117: 99 105. Holst, J. J., Christiansen, J. & Kuhl, C. 1976 ; The enteroglucagon response to intrajejunal infusion of glucose, triglycerides, and sodium chloride, and its relation to jejunal inhibition of gastric acid secretion in man. Scand. J. Gastroenterology 11: 297304. 12. Stoll, B., Chang, X., Jiang, R., Van Goudoever, J. B., Reeds, P. J. & Burrin, D. G. 2000 ; Enteral carbohydrate and lipid inhibit small intestinal proteolysis in neonatal pigs. FASEB J. 14: A558. 13. Sangild, P. T., Fowden, A. L. & Trahair, J. F. 2000 ; How does the fetal gastrointestinal tract develop in preparation for enteral nutrition after birth? Livestock Prod. Sci. 66: 141150. 14. Petersen, Y. M., Hartmann, B., Holst, J. J., Le Huerou-Luron, I., Bjornvad, C. R. & Sangild, P. T. 2003 ; Introduction of enteral food increases plasma GLP-2 and decreases GLP-2 receptor mRNA abundance during pig development. J. Nutr. 133: 17811786. 15. Sangild, P. T., Schmidt, M., Elnif, J., Bjrnvad, C. R. & Buddington, R. K. 2002 ; Prenatal development of the gastrointestinal tract in pigs and the effect of fetal gut obstruction. Pediatr. Res. 52: 416 424. Petersen, Y. M., Burrin, D. G., Schmidt, M., Hartmann, B., Holst, J. J. & Sangild, P. T. 2001 ; Glucagon-like peptide 2 has differential effects on small intestinal growth and function in fetal and neonatal pigs. Am. J. Physiol. 281: R1986 R1993. 17. Burrin, D. G., Stoll, B., Jiang, R., Petersen, Y., Elnif, Y., Buddington, R. K., Schmidt, M., Holst, J. J., Hartmann, B. & Sangild, P. T. 2000 ; GLP-2 stimulates intestinal growth by suppressing proteolysis and apoptosis in parenterally fed premature piglets. Am. J. Physiol. 279: G1249 G1256. 18. Petersen, Y. M., Elnif, J., Schmidt, M. & Sangild, P. T. 2002 ; Glucagon-like peptide 2 enhances maltase-glucoamylase and sucrase-isomaltase gene expression and activity in parenterally fed premature neonatal piglets. Pediatr. Res. 52: 498 503. Buddington, R. K., Elnif, J. & Sangild, P. T. 2000 ; Responses of the perinatal pig intestine to glucagon-like peptide 2. FASEB J. 14: A211. 20. Le Huerou-Luron, I., Petersen, Y. M., Hartmann, B., Holst, J. J. & Sangild, P. T. 2002 ; Exogenous GLP-2 has limited effects on weaning-induced intestinal adaptation in piglets. Gastroenterology, Suppl. 122, A557. 21. Nielsen, T. T., Sangild, P. T., Elnif, J., Sorensen, K., Leser, T., Holst, J. J., Hartmann, B., Jensen, B. B. & Hedemann, M. S. 2003 ; Effects of GLP-2 treatment and antibiotics on gut structure and function during pig weanling diarrhea. Proceedings of the 9th International Symposium on Digestive Physiology in Pigs, Calgary, Canada. pp. 161163. University of Alberta. 22. Burrin, D. G., Stoll, B., Chang, X., Guan, X., Hartmann, B. & Holst, J. J. 2002 ; Dose-dependent intestinal trophic effects of glucagon-like peptide 2 in TPN-fed neonatal pigs. Gastroenterology 122: A249. 23. Van Goudoever, J. B., Stoll, B., Hartmann, B., Holst, J. J., Reeds, P. J. & Burrin, D. J. 2001 ; Secretion of trophic gut peptides is not different in bolusand continuously fed piglets. J. Nutr. 131: 729 732. Zhang, H., Malo, C. & Buddington, R. K. 1997 ; Suckling induces rapid intestinal growth and changes in brush border digestive functions of newborn pigs. J. Nutr. 127: 418 426. Davis, T. A., Burrin, D. G., Fiorotto, M. L. & Nguyen, H. V. 1996 ; Protein synthesis in skeletal muscle and jejunum is more responsive to feeding in 7- than in 26-day-old pigs. Am. J. Physiol. 270: E802E809. 26. Burrin, D. G., Davis, T. A., Ebner, S., Schoknecht, P. A., Fiorotto, M. L., Reeds, P. J. & McAvoy, S. 1995 ; Nutrient-independent and nutrient-depen and exenatide.
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Balla, T., Sim, S. S., Iida, T., Choi, K. Y., Catt, K. J., and Rhee, S.G . 1991 ; J. Biol. Chem. 266, 24719-24726 Bansal, V S., and Majerus, P. W. 1990 ; Annu. Rev. Cell B i d 4147 Bemdge, M. J. 1987 ; Annu. Reu. Biochem. 56, 159-193 Berridge, M. J., and Imine, R. F. 1989 ; Nature 341, 197-204 Bonadonna, G., Bernardo, G., GiaMi, L., and della Cuna, G . R. 1988 ; Handbook ofMedica1 Oncology Bonadonna, G . , and della Cuna, G . R., eds ; pp. 335-378, Masson s.p. A., Milan, Italy Capranico, G., Zunino, F., Kohn, K. W., and Pommier, Y. 1990 ; Biochemistry 27, 562-569 Connolly, T. M., Lawing, W. J., Jr., and Majerus, P. W. 1986 ; Cell 46, 951-958 Ely, J. A., Hunyadi, L., Baukal, A. J., and Catt, K.J. 1990 ; Biochem. J. 168, 333-338 Gambetta, R. A Banti, P., Lanzi, C., Franzi, A and Zunino, F. 1989 ; ?bmori 76, 358-361 Greene, R. E , Collins, J. M., Jenkins, J. F., Speyer, J. L., and Myers, C. E. 1983 ; Cancer Res. 43, 34174421 Grynkiewicz, G., Ponie, M., and Tsien, R. Y 1985 ; B i d Chem. 280, 344&3450 . J. Guse, A. H., and Emmrich, F. 1991 ; Biol. Chem. 266, 24498-24502 J. Guse, A. H., and Emmrich, F. 1992 ; Chromatogr: 593, 157-163 J. Guse, A. H., Roth, E., and Emmrich, F. 1992 ; Biochem. J. 288, 489.495 Guse, A. H., Roth, E., and Emmrich, F. 1993 ; Biochem. J. 291, 447-451 Hill, T D., Zwiller, J., and Boynton, A. L. 1989 ; Cell. Physiol. 140, 403-407 . J. Imboden, J. B., and Weiss, A. 1987 ; Biochem. J. 247, 695-700 Imine, R. F., and Moor, R. M. 1986 ; Biochem. J. 240, 917-920 Johnson, R. M., Wasilenko, W.J., Mattingly, R. R., Weber, M. J., and Garrison, J. C. 1989 ; Science 2 6 121-124 King, W. G., and Rittenhouse, S. E. 1989 ; Biol. Chem. 264, 6070-6074 J. Lanzi, C., Banfi, P., Ravagnani, F., and Gambetta, R. A. 1988 ; Biochem. Pharmncol. 37, 3497-3504 Lanzi, C., Gambetta, R. A., Perego, P., Banfi, P., Franzi, A., Guazzoni, L., and Zunino, F. 1991 ; J . Cancer 47, 13G142 Znt. Biochem. Pharmacol. 4 , 747-753 4 Lear, L., Nation, R. L., and Stupans, I. 1992 ; Liickhoff, A., and Clapham, D. E. 1992 ; Nature 365, 35&358 Mayr, G . W. 1988 ; Biochem. J. 254, 585-591 Mayr, G . W. 1990 ; Methods in Znositide Research Imine, R. F., ed ; , pp. 83-108, Raven Press, New York McDonald, T.V , Premack, B. A., andGardner, P. 1993 ; J. Biol. Chem. 268, . 3889-3896 Murphree, S. A Tritton, T. R., Smith, P. L., and Sartorelli, A. C. 1981 ; Biochim. Biophys. Acta 649, 317-324 Neidle, S., and Sanderson, M. R. 1983 ; Molecular Aspects of Anticancer Drug Action Neidle, S., and Waring, M. J., eds ; , pp. 35-56, Maanillon Press, London Pittet, D., Lew, D. P., Mayr, G . W., Monod, A., and Schlegel, W. 1989a ; Biol. J. Chem. 264, 7251-7261 Pittet, D., Schlegel, W., Lew, D. P., Monod, A and Mayr, G. W. 1989b ; . Biol. J Chem. 264, 18489-18493 Posada, J. Vichi, P., and Tritton, T. 1989 ; Cancer Res. 49, 6634-6639 Sim, S. S., Kim, J. W., and Rhee, S. G . 1990 ; . Biol. Chem. 265, 10367-10372 J Schobitz, B., Netzker, R., Hannappel, E., and Brand, K. 1991 ; Eur J. Biochem. 199, 257-262 Tritton, T. R., and Yee, G . 1982 ; Science 217, 248-250 Weiss, A., Imboden, J., Hardy, K., Manger, B., Terhorst, C., and Stobo, J . 1986 ; Annu. Reu. Zmmunol. 4, 593419 and factive.
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