Pathologic anatomy of experimental listeriosis

The authors present a survey of the Soviet and foreign literature and findings of their own experimental studies. On the basis of these data the pathologo-anatomic picture of listerosis in laboratory animals (white mice, guinea-pigs and rabbits) is given in dynamics and histogenesis of focal changes in this disease in elucidated. The most typical feature of listerosis in animals is lesions of the kidney where focal changes in the form of granulems could be detected macroscopically at an early period and with great consistency. Several stages in its histogenesis may be discerned: I. focal necroses of hepatic cells associated with their invasion with lister Listeria; 2. appearance of cellular elements around the foci of necroses with subsequent formation of granulemas consisting mainly of leucocytes and lymphoid cells; 3. development of necrobiotic changes in the central areas of granulemas with concomitance of exudative processes; 4. organization of necrotic foci with subsequent scarring.     

Dissociation of long-term analgesia and the shuttle box escape deficit caused by inescapable shock.

Previous studies indicate that inescapably shocked rats perform poorly on a 2-way shuttlebox escape task 24 hrs after shock. Because inescapably shocked rats become analgesic upon reexposure to a small amount of shock 24 hrs after inescapable shock (IS), they are likely to be analgesic during the shuttlebox escape task. Ss receiving an equivalent amount of escapable shock display neither the escape deficit nor the analgesia. Both the analgesia and the escape deficit respond in a similar fashion to the manipulation of a variety of other variables. These findings have led to the suggestion that the analgesia (long-term analgesia) may cause the IS-produced escape deficit. However, the present 2 experiments with 72 male albino rats demonstrated that 2 pituitary manipulations that completely eliminate the analgesia have no effect on the escape deficit. Both hypophysectomy and dexamethasone administration blocked the analgesic consequences of IS but did not reduce the magnitude of the escape deficit. Therefore, the long-term analgesia produced by IS does not cause the deficit in shuttlebox escape performance displayed by inescapably shocked rats. Results indicate that the pituitary is not essential in the production of this escape deficit. (47 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

DNA cleavage, antiviral and cytotoxic reactions photosensitized by simple enediyne compounds

Very potent antibiotic antitumor natural products contain a enediyne moiety which, upon thermal activation, is capable of abstracting hydrogens from DNA. 1,6-Diphenyl-3-hexene-1,5-diyne was selected as a candidate for inducing DNA strand breaks photochemically. Easily interconverted with light, both geometric isomers 1 and 2 were expected to be phototoxic. As anticipated, they photosensitized the production of strand breaks in double-stranded supercoiled pBR322, and in single-stranded M13 DNA. The DNA cleavage reactions were favored by the presence of oxygen and were inhibited by ethanol. Preliminary experiments with the (Z)-isomer indicated moderate light-dependent antiviral activity against human immunodeficiency virus (HIV), Sindbis virus, and mouse cytomegalovirus. The enediynes were cytotoxic to Escherichia coli, a gram-negative organism, to Streptococcus faecalis, a gram-positive organism, to Daphnia magna and to fish (Pimephales promelas), but only in the presence of light. The production of o-terphenyl, the expected product of Bergman cyclization of 1, could not be confirmed. However, both 1 and 2 photosensitized the formation of singlet oxygen and of superoxide anion radical, and photodynamic reactions could have been responsible for some of the phototoxic reactions observed.     

Activation of angiotensin-generating systems in the developing rat kidney

The present study was designed to determine the developmental changes in intrarenal angiotensin (Ang) peptides in the rat. Kidney Ang I and II levels were threefold and sixfold higher in newborn than adult kidneys, respectively (Ang I, 678 +/- 180 versus 243 +/- 38 fmol/g, P < .01; Ang II, 667 +/- 75 versus 103 +/- 6 fmol/g, P < .001). Intrarenal Ang II levels correlated positively with the temporal changes in renin gene expression (r = .93, P < .001). However, no correlation was found between renal Ang II content and angiotensin-converting enzyme (ACE) expression during development, which prompted us to evaluate whether renal enzymes, other than renin and ACE, contribute to Ang II formation in the developing kidney. Angiotensin peptide levels were measured in newborn and adult kidney homogenates incubated with human angiotensinogen (a poor rat renin substrate) for 30 minutes at 37 degrees C. Inhibitors of aspartyl proteases and metalloproteases were ineffective in preventing the formation of Ang II in either newborn or adult kidneys. However, addition of the serine protease inhibitors soybean trypsin inhibitor and phenylmethylsulfonyl fluoride inhibited Ang II generation in the newborn kidneys only. In contrast, Ang I generation was not affected by inhibition of serine proteases in either newborn or adult kidneys. We conclude that Ang I and II synthesis is activated in the developing rat kidney. In addition to renin and ACE, the newborn rat kidney expresses serine protease activity that is capable of generating Ang II directly from angiotensinogen. This putative enzyme is induced in the newborn kidney and may cooperate with renin in the activation of Ang II synthesis during early development.