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עמוד בית
Fri, 19.07.24

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December 2004
R. Ness-Abramof, D. Nabriski and C.M. Apovian

The prevalence of obesity worldwide has risen sharply during the last four decades. The etiology of obesity is complex and includes a host of genetic influences in addition to the overconsumption of energy coupled with a sedentary lifestyle. Obesity is known to cause or exacerbate many co-morbid conditions such as diabetes, hypertension, dyslipidemia, coronary heart disease, stroke, certain cancers, arthritis and obstructive sleep apnea. Modest weight losses of 5–10% of actual weight are related to significant improvements in co-morbid conditions, but unfortunately the rate of recidivism with short-term therapy for obesity is high. The recent recognition of obesity as a chronic disease that should be treated with long-term programs and possibly with polypharmacy, and the alarming increase in its prevalence, have prompted extensive research and the development of new pharmacotherapy.

S. Stahl, E. Bar-Meir, E. Friedman, E. Regev, A. Orenstein and E. Winkler

Melanoma is the leading cause of death from skin tumors worldwide, with an annual increase in incidence over the past decade. The molecular mechanisms involved in melanoma pathogenesis are beginning to be unraveled. While a family history of melanoma and exposure to ultraviolet irradiation have been known for years as risk factors in melanoma development, the precise genes involved in inherited predisposition were defined only in the past decade. Germline mutations in two genes that play a pivotal role in controlling cell cycle and division – CDKN2A and cyclin-dependent kinase 4 (CDK4) – have been detected in autosomal, dominant, high penetrance familial melanoma cases. In addition to these two highly penetrant genes, germline mutations and polymorphisms in a few low penetrance genes have been reported in familial melanoma cases: melanocortin-1 receptor, epidermal growth factor, glutathione s-transferase M1, cytochrome p450 debrisoquine hydroxylase locus (CYP2D6) and vitamin D receptor.

E. Zebeede, U. Levinger and A. Weinberger
November 2004
F.F. Simonstein

While some claim that germ-line engineering is a definite possibility, the law in Israel and in most countries states that it should be avoided. This paper suggests that using GLE[1] in order to ‘self-evolve’ (when it becomes safe) is not only inevitable but also morally justified. This paper argues that,  


  • The great achievements of healthcare during the last century, enabling longer life, have made almost everyone prey to late-onset diseases.

  • The conundrum of healthcare allocation is worsening, partly due to late-onset dysfunctional genes that have escaped the barriers of natural selection.

  • Trying to free future generations from late-onset diseases (such as Alzheimer’s for instance) may be considered as ‘eugenics’ but, if pursued freely and justly, is a noble goal.

  • We will be affecting future generations whether or not we use GLE.

  • By definition, GLE might be reversible; it follows therefore that GLE may not necessarily represent the dramatic change inserted in the germ line forever – as is usually suggested.

  • Reproductive freedom and justice are paramount in this scenario. These values are not necessarily incompatible if the right policies are in place.






[1] GLE = germ line engineering


A.B. Jotkowitz, A. Porath and S. Glick
M. Leitman, V. Shir, E. Peleg, S. Rosenblatt, E. Sucher, R. Krakover, E. Kaluski and Z. Vered

Background: Cardiac rupture is a rare but ominous complication of myocardial infarction.

Objectives: To study the clinical presentation, medical course, outcome and echocardiographic predictors of patients with myocardial rupture.

Methods: We evaluated 15 consecutive patients with cardiac rupture during a 4 year period in our department. The current report explores the presence of potential risk factors, timing, relation to the thrombolysis, coronary interventions and outcome.

Results: The index event in all patients was first ST elevation myocardial infarction. In seven patients rupture occurred in the first 24 hours. Pericardial effusion on admission with a clot was present in three patients. Five patients received thrombolytic therapy. Only three patients underwent coronary angioplasty, but in one case it was performed late and in two patients the culprit artery could not be opened. Six patients reached the operating room, of whom three survived.

Conclusions: The lack of early mechanical reperfusion in acute myocardial infarction and thrombolytic therapy are risk factors for cardiac rupture. Pericardial effusion on admission and evidence of a clot are echocardiographic indicators of cardiac rupture and should alert the medical team to further assess the possibility of cardiac rupture.
 

N. Hiller, O. Goitein and Y.J. Ashkenazi
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