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עמוד בית
Thu, 18.07.24

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December 2000
Rosalie Ber, MD, DSc, Gershon B. Grunfeld, PhD and Gideon Alroy, MD
 The Rappaport Faculty of Medicine of the Technion established an Ethics in Medicine Forum in March 1993. The main objective of the forum was to increase awareness of the philosophical principles of ethics in medicine, as defined and developed in the western world during the last three decades. The multidisciplinary forum meets once a month during the academic year. Our 7 years experience is documented. Of the 45 meetings, 30 were clinically oriented and of these more than half were based on cases. Only 15 meetings were purely theoretical. Our principal a assumption was that any and every topic could be discussed, including those covered by the law We explored a how well western philosophical principles and rules fit the Israeli picture. Many of the forum discussions related to 0 the draft of the Patient’s Bill of Rights which came into effect on 12 May 1996. The role of the ‘legal’ hospital ethics committees was compared to that of the “advisory” ethics committees whose members constituted a large share of our forum. The multicultural Israeli population and the practice of medicine therein raised many lively discussions. The principle of autonomy in the ultra-orthodox and in the family setting was a highly controversial issue. The forum served as a workshop for examining traditional medical ethical principles, which we strongly feel needs to he amended in light of the 1996 Patient’s Bill of Rights. From our 7 years experience with an Ethics in Medicine Forum we recommend that medical ethical deliberations focus on genuine medical cases.

November 2000
Oded Szold MD, Avi A. Weinbroum MD, Ron Ben-Abraham MD, Talma E. Englender MD, Dror Ovadia MD and Patrick Sorkine MD

Background: Tumor necrosis factor is associated with various local and systemic inflammatory sequelae following snakebite. Xanthine oxidase is a principal mediator of remote tissue injury (e.g., lungs, heart, liver).

Objective: To investigate in a snakebite-like animal model the as yet unexplored role of TNF and XO in mediating organ damage following snakebite.

Methods: Sprague-Dawley rats were injected intramuscularly with a non-lethal 500 g/kg dose of Vipera aspis venom (n=10) or saline (n=10). Blood pressure and heart rate were continuously monitored, TNF- was measured in the blood, and total XO + xanthine dehydrogenase activity was assessed in various tissues. Lung histology and permeability indices were analyzed.

Results: Venom injection caused a significant (P0.05) reduction in both heart rate and invasive arterial pressure. The blood circulating TNF levels were significantly higher in the intoxicated group (P0.05 vs. saline group), with changes seen at 30 minutes from intoxication in both groups. Total XO + XDH activity in the kidney, lung and liver of the venom-injected group was significantly (P0.05) higher than in the saline group, while the activity in the heart was similar.

Conclusions: The mediation of remote organ and hemodynamic changes following intramuscular injection of a non-lethal dose of Vipera aspis venom can be attributed partly to TNF and partly to XO. More research is needed to better understand the role of either compound and the time frame of their activity before specific antagonists can be introduced for snakebite management.
 

David Peleg MD, Aviva Peleg MSc and Eliezer Shalev MD

Background: Human chorionic gonadotropin, the pregnancy hormone, is synthesized by trophoblast cells which make up the placenta.

Objective: To determine whether antibody to hCG can be used to specifically detect living trophoblast in vitro by binding to the external membrane.

Methods: Trophoblast was isolated from fresh placentas of women undergoing termination of pregnancy in the first trimester and incubated with monoclonal antibody to hCG. Anti-mouse immunoglobulin G with a fluorescent marker was then added.

Results: Syncytiotrophoblast stained positive on the external surface of the cell, while controls of leukocytes, endometrial cells and hepatocytes were negative.

Conclusion: The hCG monoclonal antibody may be used to specifically detect hCG on the surface of living trophoblast in vitro.
 

by Fabrizio Conti, MD, Francesca Romana Spinelli, MD, Alejandra Ossandon, MD and Guido Valesini, MD
Edward Ramadan, MD, Don Kristt, MD, Dan Alper, MD, Aliza Zeidman, MD, Tal H. Vishne, MD and Zeev Dreznik, MD
Maher Dagash, MD, Farid Nakhoul, MD, Deeb Daoud, MD, Tony Hayek, MD and Jacob Green, MD
October 2000
Valentin Fulga MD, Ben-Ami Sela PhD and Michael Belkin MA MD

Background: Most corneal damage induced by contact lenses is due to interference with corneal oxygenation.

Objective: To investigate the effect on the rabbit cornea of a rigid gas-permeable contact lens with a newly designed periphery.

Method: We fitted New Zealand white rabbits (n=12) with RGP[1] contact lenses that were identical in all respects except for the design of the periphery. In each animal, one contact lens had an innovative periphery consisting of a microscopic diffractive relief lathed on the back surface; the other contact lens was of a conventional design. The lenses were worn continuously for 7 days. During this experimental period and for 1 additional week we assessed the corneal damage by daily testing lactic dehydrogenase activity in the tears.

Results: On the last day of the experimental week and the first 3 days of the healing period, mean tear LDH[2] activity was significantly lower in the eyes with the new contact lens design than in eyes with the conventional lenses.

Conclusions: The novel periphery design reduces corneal damage resulting from contact lens wear, as reflected by LDH levels in the tears. The new design probably facilitates the flow and exchange of tears under the contact lens, resulting in improved metabolism of the cornea. These findings may also prove applicable to soft contact lenses.






[1] RGP = rigid gas permeable



[2] LDH = lactic dehydrogenase


Michael Blumenthal, MD and Moshe Schwartz, OD
Raana Shamir, MD, Aaron Lerner, MD, MHA and Edward A. Fisher, MD, PhD
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