Biography:

In the past Aryeh Hurwitz has collaborated on articles with David M. Pinson and J.David Innis. One of their most recent publications is Alimentary tractDrug-induced hypergastrinemia: Absence of trophic effects on colonic carcinoma in rats☆. Which was published in journal Gastroenterology.

More information about Aryeh Hurwitz research including statistics on their citations can be found on their Copernicus Academic profile page.

Aryeh Hurwitz's Articles: (4)

Alimentary tractDrug-induced hypergastrinemia: Absence of trophic effects on colonic carcinoma in rats☆

AbstractBackground/Aims: Published studies suggest that hypergastrinemia stimulates growth of normal or malignant colon tissue. Other studies dispute these findings. This study was designed to test the hypothesis that hypergastrinemia enhances progression or invasiveness of colon cancer. Methods: Colonic carcinomas were induced in male Sprague-Dawley rats by six weekly intraperitoneal injections of methylazoxymethanol. Four weeks after the last injection of carcinogen, the animals were randomized into four treatment groups, including vehicle control, low- and high-dose omeprazole, and ranitidine. After 10 weeks of treatment, the animals were bled, stomach weights were recorded, and colon tumors were mapped, enumerated, measured, and scored histopathologically by Dukes' classification. Crypt and mucosal heights were determined in colonic mucosa unaffected by tumor. Results: Drug administration induced a sustained hypergastrinemia that did not enhance tumor burden or invasiveness or crypt height/mucosal height ratios. Ranitidine-treated rats consumed less food, weighed less, and developed fewer tumors. This group also had lower crypt and mucosal heights than rats in the vehicleor omeprazole-treated rats. Conclusions: The results suggest that endogenous hypergastrinemia induced by these acid-suppressing drugs has no stimulatory effect on colon mucosal growth or progression or biological behavior of experimental rat colon cancer.

Mechanism of hematocrit increase induced by the combined administration of morphine and Adriamycin: Role of histamine release☆

AbstractThe mechanism by which morphine interacts with Adriamycin to increase hematocrit has been investigated in mice. Treatment with Adriamycin (12.8 mg/kg, iv) or morphine (20 mg/kg, sc) resulted in slight increases in hematocrit 30 min postdose, while animals given sc morphine 30 min prior to iv Adriamycin exhibited significant increases in hematocrit as early as 1 min post-Adriamycin. The hematocrit increase reached maximal levels 12 min post-Adriamycin and returned to basal values 4 hr postdose. Splenectomizing animals prior to morphine and Adriamycin treatment had no effect on the drug-induced hematocrit increase. This indicates that red cell release from splenic contracture is not the mechanism for the hematocrit increase. Measurement of plasma histamine levels following drug treatment demonstrated a marked and rapid rise in plasma histamine levels reaching maximal values 1 min post-Adriamycin. Adriamycin alone triggered this release; however, morphine pretreatment resulted in a higher maximum and more prolonged elevation of plasma histamine levels. Treatment with pyrilamine (3.1–50 mg/kg, ip) prior to morphine and Adriamycin administration partially reversed drug-induced hematocrit increase and protected against resultant lethality. Cimetidine (50–200 mg/kg, ip) treatment was not effective. The temporal relationship between hematocrit and histamine increases suggests a cause/effect relationship between released histamine and hematocrit elevation. Protection by pyrilamine and not cimetidine further supports this cause/effect relationship and indicates the effect is mediated via histamine type 1 receptors.

Regular articleInteraction of clonidine and morphine with lidocaine in mice and rats

AbstractMorphine and clinidine both elevated plasma levels of lidocaine to the same extent in mice while slowing lidocaine metabolism to deethylated products. The effects of clonidine on lidocaine disposition were reversed by yohimbine. Mice given morphine, 20 mg/kg sc, or clonidine, 0.2 mg/kg sc, had similar, 30–50%, elevation of plasma lidocaine levels at 15 min after lidocaine, 15 mg/kg iv, when compared to saline-treated animals. Despite similarity of effect on plasma lidocaine, mice treated with morphine were much more susceptible to lethal effects of lidocaine than were mice given clonidine. Ativ doses of 22 mg/kg or higher, lidocaine caused death in nearly all morphine-treated mice, while even 32 mg/kg lidocaine caused only 11% mortality after saline or clonidine. Clonidine, 0.5 mg/kg sc, and morphine, 20 mg/kg sc, both raised plasma lidocaine levels in rats, but only morphine depressed respiration, causing hypoxia, hypercapnia, and acidosis and increasing lidocaine lethality. These data suggest that potentiation of lidocaine toxicity by morphine is due primarily to changes in blood gases rather than to elevation in lidocaine levels.

Multiple comparisons and nonparametric statistical tests on a programmable calculator

AbstractCalculator programs are provided for statistical tests for comparing groups of data. These tests can be applied when t-tests are inappropriate, as for multiple comparisons, or for evaluating groups of data that are not distributed normally or have unequal variances. The programs, designed to run on the least expensive Hewlett-Packard programmable scientific calculator, Model HP-11C, should place these statistical tests within easy reach of most students and investigators.

Advertisement
Join Copernicus Academic and get access to over 12 million papers authored by 7+ million academics.
Join for free!

Contact us