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עמוד בית
Sun, 21.04.24

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April 2013
J.H. Spungen, R. Goldsmith, Z. Stahl and R. Reifen
 Background: Desalination of seawater and brackish water (mixed seawater and freshwater) provides an increasing portion of the Israeli drinking water supply. However, desalinated water contains little calcium (Ca) and magnesium (Mg), and consumers may be at risk for deficiencies of these essential minerals.

Objectives: To assess intakes of Mg and Ca from water, other beverages, and food in communities with different water supplies, and assess the proportion of individuals with intakes below the estimated average requirement (EAR).

Methods: Telephone interviews were conducted using a food frequency questionnaire to assess Mg and Ca intakes by adults in four communities. The proportion of individuals with Mg and Ca intakes below the EAR were evaluated based on current intakes and on potential intakes assuming that desalinated water had been introduced countrywide.

Results: The proportion of individuals with Mg intake below the EAR was higher in Kibbutz Maagan Michael (30.6%), an agricultural settlement supplied with desalinated water, than in Hadera (16.7%), a city supplied by the National Water Carrier (NWC) (P < 0.01). The proportion of individuals with Ca intake below the EAR was higher in Maagan Michael (15.3%) than in the communities supplied with water from the NWC or mixed water (27.7%–33.8%), P < 0.02.

Conclusions: Returning Mg and Ca to desalinated water may be beneficial for raising intakes in Israeli communities supplied with desalinated water. Individuals with intake of Mg and/or Ca below the EAR may be at risk for cardiac abnormalities and other medical conditions.

February 2010
B. Weiss, I. Barshack, N. Onaca, I. Goldberg, Z. Berkovich, E. Melzer, A. Jonas and R. Reifen

Background: Vitamin A and its derivative retinoic acid regulate various aspects of cell behavior as growth, differentiation, and proliferation. Retinoic acid derivatives have been suggested to play a role in processes such as hepatic regeneration and fibrosis.

Objectives: To evaluate the influence of vitamin A on rat liver epithelial cell proliferation.

Methods: We performed common bile duct ligation in rats that had been subjected to differing vitamin A diets and compared their livers to control rats. Proliferation, apoptosis, and retinoic acid receptors were evaluated by histology and immunohistochemistry in bile duct cells and hepatocytes.

Results: Vitamin A deficiency was found to be associated with enhanced proliferation of bile duct epithelial cells following CBD[1] ligation. The proliferation was manifested by increased numbers of ducts, by aberrant extended ductal morphology, and by elevated numbers of nuclei expressing the proliferation marker Ki67. The amount of vitamin A in the rat diet did not affect detectably ductal cell apoptosis. We observed up-regulated expression of the retinoid X receptor-alpha in the biliary epithelium of vitamin A-deficient rats that had undergone CBD ligation, but not in vitamin A-sufficient rats.

Conclusions: We speculate that the mechanism underlying the ductal proliferation response involves differential expression of RXR[2]-alpha. Our observations suggest that deficiency of vitamin A may exacerbate cholestasis, due to excessive intrahepatic bile duct proliferation.






[1] CBD = common bile duct



[2] RXR = retinoid X receptor


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.

February 2000
Arie Levine MD, Yoram Bujanover MD, Shimon Reif MD, Svetlana Gass, Nurit Vardinon, Ram Reifen MD and Dan Lehmann PhD

Background: Anti-endomysial antibodies are sensitive and specific markers for celiac disease. This antibody has recently been identified as an antibody to tissue transglutaminase, an enzyme that cross-links and stabilizes extracellular matrix proteins.

Objectives: To evaluate the clinical usefulness of an enzyme-linked immunoassay for anti-transglutaminase antibodies, and to compare the results with those of AEA, the current gold standard serological test for celiac disease.

Methods: Serum samples were collected from 33 patients with biopsy-proven celiac disease and AEA tests were performed. Control samples for anti-transglutaminase were obtained from 155 patients. An ELISA test for immunoglobulin A anti-transglutaminase utilizing guinea pig liver transglutaminase was developed and performed on all sera.  Cutoff values for the test were performed using logistic regression and receiver operating curves analysis.

Results: An optical density cutoff value of 0.34 was established for the assay. The mean value was 0.18±0.19 optical density for controls, and 1.65±1.14 for patients with celiac disease (P<0.001). Sensitivity and specificity of the assay were both 90%, while AEA had a sensitivity and specificity of 100% and 94%, respectively.

Conclusions: A tissue transglutaminase-based ELISA test is both sensitive and specific for  detection of celiac disease.

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AEA = anti-endomysial antibody

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