Jack Yehudi Vanderhoek

The Jewish community in The Netherlands dates from the end of the 16th century when Portuguese and Spanish Conversos, fleeing the Iberian Inquisition, first received approval from the Amsterdam aut...

Major improvements in medical diagnostics and treatments in Dutch hospital care during the second half of the 19th century led to a shift from a nearly exclusive focus on indigent patients to an increasing proportion of hospital beds dedicated to paying middle-class patients. To accommodate this change, three private non-sectarian hospitals for middle-class patients were established in Amsterdam between 1857 and 1902. However, the two Jewish hospitals in the Dutch capital, the Dutch Jewish Ashkenazi hospital (NIZ), and the Portuguese Jewish hospital (PIZ), initially established exclusively for poor Jews, were much slower to respond to the trend of increasing hospital care for the middle class. This study examines how these hospitals addressed the needs of both poor and middle-class patients in the first decades of the 20th century as well as the success of the Centrale Israelitische Ziekenverpleging (CIZ, Central Jewish hospital) that was established solely for middle-class Jewish patients. The report also investigates how, after the devastation of the Amsterdam Jewish community during WW2, the CIZ managed to remain and today is the only ritually observant Jewish hospital unit in the Netherlands.

The Joles Jewish Hospital in Haarlem (a small city in the Netherlands) was established in 1930 to provide a Jewish milieu for local patients. Mozes Joles, a wealthy Jewish businessman, bequeathed his fortune to the Haarlem Jewish community to accomplish this objective, and its spiritual leader, Rabbi Simon Philip de Vries, was the driving force in successfully achieving this goal. The Joles Hospital was forcibly closed by the Nazis in 1943, and the postwar leadership of the Haarlem Jewish community decided not to reopen it. Instead, they used the Joles inheritance to build old age homes in both Haifa, Israel, and Haarlem, thus ensuring a Jewish environment for elderly care in both locales. The realization of one man’s charitable act bettered the lives of both ill and elderly individuals.

The development of the modern hospital is usually dated to the nineteenth century. During this time, many municipal and sectarian hospitals were established and developed, and Jewish hospitals were no exception. Such developments also occurred in the Netherlands. This essay describes the different histories of the Jewish hospitals in Rotterdam and The Hague during the nineteenth century. The Rotterdam institution lasted for more than 130 years (until it was closed by the Nazis during the Second World War), whereas the one in The Hague existed for only 31 years. This study will suggest a number of possible explanations for the relatively long and successful history of the Jewish hospital in Rotterdam and the contrastingly brief duration of the Jewish hospital in The Hague.

In the early seventeenth century, the Jews formally established two separate communities in Amsterdam, the Portuguese Sephardi and the High German Ashkenazi congregations. Until the end of the eighteenth century, medical care for the Amsterdam indigent Jews had been controlled and regulated by the powerful Parnasim, the de facto rulers, of each community. The primary communal organizations that were exclusively responsible for medical care for the poor were the Bikur Holim societies. This approach for the care of the indigent Jewish sick became ineffective in the nineteenth century and was replaced by a hospital-based system. This essay describes how seriously ill indigent Jews in nineteenth-century Amsterdam received hospital care, tracing the establishment and development of the first Ashkenazi and Sephardi hospitals in the city. Although each community established their own hospital, they used different approaches to accomplish this goal.

Lipid profiles of seven human breast milk samples obtained from milk banks and four infant formulas were compared in view of the potential food hypersensitivities of certain infants to human milk.The cholesterol (0.15-0.26 mM) content of the human samples was about 50% lower than that found in the infant formulas whereas the triglyceride (TG, 173-386 mM) contents of these products were found to be comparable.The major saturated fatty acid (SFA) and mono-unsaturated fatty acid (MUFA) were 16:0 and 18:1 respectively. The major poly-unsaturated fatty acid (PUFA) was 18:2 with other PUFA members of the C18, C20 and C22 families identified and quantified. Although conjugated linoleic acid (CLA) was not detected in any infant formulas tested, no other major differences in the fatty acid patterns were found. However, the mean (13.6) of the ratio of n-6 PUFAs/n-3 PUFAs in the human milk samples was about 50% higher than that observed in the infant formula samples.Although our results indicate that there are small yet significant differences in cholesterol and CLA content and the ratio of n-6 PUFAs/n-3PUFAs, the lipid composition of milk bank breast milk and infant formulas is quite comparable.

This study examined the effects of five CLA isomers and the non‐conjugated LA on nitric oxide (NO) production, an important modulator of vasodilation, inflammation, and cytotoxicity. Bovine aortic endothelial cells (BAECs) were pretreated with pure CLAs (c9, c11‐, c9, t11‐, t9, t11‐, t10, c12‐, c11, c13‐CLA) and the non‐conjugated c9, c12‐analog, then stimulated by the ionophore A23187 followed by fluorescence monitoring of NO production. CLAs (5 μM) decreased NO formation in the range of 20–40% relative to non‐fatty acid‐treated controls with the t9, t11‐ and t10, c12‐CLAs being the most effective. The inhibitory effect of either of these CLAs was not time dependent over a 120 min time interval. Phosphatidylcholine (PC) and phosphatidylethanolamine (PE) play crucial roles in membrane structure and cell signaling. Since CLAs are usually esterified in these phospholipids (PLs), the effects of three CLA‐containing PLs and 2‐linoleoyl‐PC on NO production by A23187‐stimulated BAECs were also examined. c9, t11‐CLA‐PC and 2‐linoleoyl‐PC dose‐dependently inhibited NO production over a 60–1,000 μM concentration range whereas c9, c11‐CLA‐PC and c9, t11‐CLA‐PE were ineffective. Both c9, t11‐CLA‐PC and linoleoyl‐PC exhibited a time‐dependent decrease in NO production from 5 to 120 min. The results of the present study suggest that the influence of several C18 polyunsaturated fatty acids incorporated into cellular phospholipids on the A23187‐induced formation of NO by BAECs is strongly dependent on the positional and geometric nature of the double bonds.

Endothelial cell function can be influenced by nutrition, especially dietary FA and antioxidants. One class of dietary FA that is found in meat and dairy products derived from ruminant animals is conjugated linoleic acids (CLA). We have examined the effects of several CLA isomers on endothelial cell proliferation. 9t,11t‐CLA was the only isomer that inhibited bovine arotic endothelial cell (BAEC) [³H]methylthymidine incorporation (I₅₀=35 μM), and this antiproliferative effect was time‐dependent. A small decrease (20%) in cell number was observed only at the highest concentration (60 μM) tested. The 9c,11t‐, 9c,11c‐, 10t 12c‐, and 11c,13t‐CLA isomers did not exhibit any antiproliferative effects over a 5–60 μM concentration range. α‐Tocopherol and BHT decreased BAEC proliferation, but pretreatment of cells with either of these antioxidants substantially attenuated the antiproliferative effect of 9t,11t‐CLA. No difference in lipid peroxidation, as measured by the thiobarbituric acid assay for malondialdehyde, was observed on treatment of endothelial cells with either 9t,11t‐ or 9c,11t‐CLA. However, a 43% increase in caspase‐3 activity was observed after incubating BAEC with 9t,11t‐CLA, suggesting that the antiproliferative effect of this isomer is partially due to an apoptotic pathway. In contrast to the above results with normal endothelial cells, these five CLA isomers all inhibited proliferation of the human leukemic cell line THP‐1, with the 9t,11t isomer again being the most (I₅₀=60 μM) effective. These results confirm that different CLA isomers have different inhibitory potencies on the proliferation of normal and leukemic cells.