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עמוד בית
Thu, 21.11.24

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March 2007
A. Brautbar, Y. Esyag, G.S Breuer, Y. Wiener-Well and G. Nesher

The human papillomavirus family of viruses causes a variety of benign, premalignant and malignant lesions in men and women. All cervical cancers are caused by HPV[1]. It is the leading cause of death from cancer in women in developing countries; every year some 493,000 women develop cervical cancer and 230,000 women die every year of this disease. The vaccine against HPV includes virus-like particles, composed of the major viral capsid protein of HPV without the carcinogenic genetic core. Large-scale studies have shown that the vaccine is tolerated well, leads to high antibody levels in both men and women, and prevents chronic HPV infection and its associated diseases. To achieve effective coverage the vaccine should be given prior to sexual debut. Introduction of the vaccine into specific countries, particularly Israel, should take into account the local incidence of cervical cancer as well as the increasing incidence of precancerous cervical lesions and genital warts, which reduce quality of life and are associated with considerable costs.

 

 







[1] HPV = human papillomavirus


November 2005
J. Delgado, A.D. Sperber, V. Novack, B. Delgado, L. Edelman, N. Gaspar, P. Krugliak, S. Odes, A.B. Jotkowitz, M. Faszczyk and A. Fich
 Background: The epidemiology of primary biliary cirrhosis has changed significantly over the last decade, with a trend towards increasing prevalence in many places around the world.

Objectives: To determine the overall prevalence of PBC[1] in southern Israel and the specific rates for different immigrant groups between January 1993 and October 2004.

Methods: Multiple case-finding methods were used to identify all cases of PBC in the study region. Age-adjusted prevalence rates were compared among the different immigrant groups.

Results: A total of 47 cases of PBC were identified with an overall prevalence of 55 cases per million. All patients were women, and all except for a Bedouin Arab were Jewish. Foreign-born patients comprised 70% of our PBC cohort even though they represent only 45.4% of the regional population. This predominance of immigrants did not change when the rates were adjusted for age (P < 0.001). The prevalence rates were 40, 177, and 58 cases per million for those born in Israel, North Africa or Asia, and Eastern Europe, respectively. The age-specific prevalence rate for women older than 40 years varied from 135 cases per million among those born in Israel to 450 among immigrants from Eastern Europe and the former USSR to 700 cases per million among immigrants from North Africa and Asia.

Conclusions: The prevalence of PBC in southern Israel is similar to that reported from some European countries. The rate is much higher among Jews than Arabs and among immigrants to Israel compared to native Israelis.


 



[1] PBC = primary biliary cirrhosis


April 2005
J. Kogan, S. Turkot, B. Golzman and S. Oren
Background: Hemodynamic changes, including systemic vascular resistance, in cirrhotic patients during massive paracentesis have been reported, but large and small artery compliance has not yet been investigated.

Objective: To investigate hemodynamic variables, including small and large artery compliance, in cirrhotic patients during total paracentesis.

Methods: The study included 15 cirrhotic patients admitted for an episode of tense diuretic-resistant ascites. Hemodynamic variables including vascular compliance were measured using an HDI pulse wave cardiovascular profiling instrument CR-2000. The variables were measured in these patients before, immediately after and 24 hours following large volume (mean 5.6 L) paracentesis.

Results: Cardiac output increased immediately after paracentesis due to increment in stroke volume, with no change in heart rate. However, 24 hours later the cardiac output decreased to below the basal level. The fluctuation was statistically significant (P < 0.05). There was no change in large artery compliance, but small artery compliance increased after paracentesis (P < 0.05) and partially returned to the basal level after 24 hours. Systemic vascular resistance measurement showed the same pattern of change: vasodilatation occurred during paracentesis and was attenuated 24 hours later.

Conclusions: Large volume paracentesis with albumin replacement caused an accentuation of the vasodilatation (small but not large artery) already present in these patients. This may be the first sign of enhanced vasodilatation due to large volume paracentesis before the clinical expression of impaired hemodynamics and deterioration of renal function.

November 2003
December 2002
June 2001
Carmi Bartal, MD, Maximo Maislos, MD, Doron Zilberman, MD and Emanuel Sikuler, MD
February 2001
Joram Wardi, MD, Ram Reifen, MD, Hussein Aeed, PhD, Liliana Zadel, MD, Yona Avni, MD and Rafael Bruck, MD

Objective: To study whether retinolpalmitate, beta-car­otene or lycopene could prevent liver cirrhosis induced by thioacetamide in rats.

Methods: In the control group liver cirrhosis was induced in male Wistar rats by intraperitoneal injections of TAA 200 mg/ kg for 12 weeks. The three study groups received in addition to TM either beta-carotene, lycopene or retinolpalmitate by gavage through an orogastric tube. Histopathological analysis and determination of the hydroxyproline contents of the livers were performed at the end of the protocol.

Results: Rats treated with beta-carotene and TAA had lower histopathologic scores and reduced levels of hepatic hydroxyproline (P= 0.02) than those treated by TAA alone. A trend of decreased fibrosis was observed in the rats treated with lycopene and TAA although this lacked statistical significance.

Conclusions: Beta-carotene attenuated liver cirrhosis induced by TAA in rats. The mechanism may be related to effects on hepatic stellate cells or to scavenging of free radicals by beta-carotene. Retinolpalmitate and lycopen had no significant beneficial effect.

September 1999
Sandra Reynoso-Paz, MD, Ross L. Coppel, MD, Aftab A. Ansari MD, and M.Eric Gershwin, MD
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