[ effect of carbenoxolone on morphine-induced withdrawal symptoms in rats]

The exact mechanisms of morphine dependence and withdrawal syndrome remain unclear. Many studies have been performed to find a drug for prevention of withdrawal syndrome. The aim of this study was to evaluate the effect of carbenoxolone [a gap junction inhibitor] on morphine withdrawal syndrome in male rats. In this experimental study, adult male Sprague Dawley rats with weights between 225 and 275 g were selected randomly and divided into 8 groups. Each group consisted of 8 rats. In order to induce dependency, morphine was injected subcutaneously for nine days [1[st] day: 5mg/kg, 2[nd] and 3[rd] days: 10 mg/kg, 4[th] and 5[th] days: 15 mg/kg, 6[th] and 7[th] days: 20 mg/kg, 8[th] and 9[th] days: 25 mg/kg]. On the ninth day only the morning dose of morphine was injected, then control group and treatment groups received IP injection of saline [1 ml/kg] and IP injection of carbenoxolone [5, 25, 50, 100 mg/kg] respectively. After 30 min all groups received IP injection of naloxone [4 mg/kg] and the withdrawal signs including: jumping, rearing, genital grooming, abdominal writhing, body grooming and wet dog shake, were recorded for 60 minutes. Our results showed that carbenoxolone not only decreased all withdrawal signs, but also reduced the total withdrawal scores, significantly. In conclusion we found that carbenoxolone as a gap junction inhibitor was effective in decreasing the symptoms of morphine withdrawal syndrome.

Aminoglycosides modifying enzymes genes among the population of enterococci in Tehran

Resistance to high level concentration of gentamicin is widespread among isolates of enterococci at Tehran Hospitals. To understand the mechanism of resistance among the Iranian isolates, we screened a collection of E. faecalis and E. faecium isolates to detect aminoglycoside modifying enzymes genes. To detect the high level gentamicin resistant isolates of enterococci [HLGR phenotype, MIC>500 microg/ml], 114 clinical isolates of E.faecalis [n=79] and E. faecium [n=35] were tested with disks containing 120 microg of gentamicin. The macrobroth dilution assay was then used to determine the minimum inhibitory concentration of gentamicin. The susceptibility of isolates against amikacin, netilmicin, tobramycin, kanamycin were also determined by Kirby-Bauer method. All isolates were subjected to polymerase chain reaction assays targeting aminoglycoside modifying enzyme [AMEs] genes including aac [6']-aph [2"], aph [2"]-Ib, aph [2"]-Ic, aph [2"]-Ia, aph [2"]-Id. Aph[3']-IIIa and ant [4']-Ia. All isolates with HLGR phenotype and those showing 64