Facial restoration after trauma - nasolabial in monkey bugio - Alouatta caraya (Humboldt, 1812) - first case report / [Restauração facial pós trauma nasolabial em macaco bugio - Alouatta caraya (Humboldt, 1812) - relato de caso]

In the last decades in the State of Mato Grosso do Sul - Brazil, the reduction in the preservation of areas due to the degradation of the biome and destruction of the natural environment has caused animals, mainly in the order of non-human primates, to come closer to towns and highways, increasing the number of accidents and in some cases, deaths. New surgical techniques have been developed that favor these species as explained in this report. The howler monkey patient was traumatized in the facial region damaging important vital structures such as facial muscle groups responsible for swallowing food, chewing, breathing, defense, and communication (vocalization and mimicry), in addition to the cartilaginous nasal structures. However, reconstructive facial surgical techniques, used on humans, showed satisfactory results from an anatomical, functional, and aesthetic point of view in howler monkey, with acceptance of the animal with a safe postoperative period for a full recovery of the primate patient.(AU)

Nas últimas décadas, no estado do Mato Grosso do Sul - Brasil, a redução de áreas preservadas pela degradação de biomas e pela destruição de habitat naturais tem favorecido a aproximação de animais - muitos desses, primatas não humanos - em cidades e rodovias, aumentando o número de acidentes e, em alguns casos, de mortes. Novas técnicas cirúrgicas têm sido desenvolvidas, favorecendo essas espécies, como reportado neste trabalho. O paciente macaco bugio foi traumatizado em região facial, envolvendo importantes estruturas vitais, como grupos musculares faciais responsáveis pela apreensão alimentar, mastigação, respiração, defesa e comunicação (vocalização e mímicas), além das estruturas cartilaginosas nasais. No entanto, técnicas cirúrgicas reconstrutivas em face aplicadas e descritas em humanos apresentaram resultados satisfatórios dos pontos de vista anatômico, fisiológico e visual nos macacos bugio, com aceitação deles diante do estresse, com pós-operatório seguro, resultando na reabilitação do paciente primata.(AU)

Apoptotic vs. nonapoptotic cytotoxicity induced by hydrogen peroxide.

The regulation of cellular cytotoxicity induced by hydrogen peroxide (H2O2) over a wide concentration range was assessed. Three distinct patterns were detected: the highest concentrations (> 10 mM) rapidly induced a necrotic form of death characterized by smeared patterns of DNA digestion and morphological evidence of primary cytoplasm and plasma membrane damage; In contrast, 10 and 5 mM H2O2 induced endonucleosomal DNA digestion concurrently with cytotoxicity and target cell death was associated with morphologic evidence of apoptosis. Apoptosis was inhibited by cycloheximide, emetine, aminobenzamide (ABA), aurintricarboxylic acid, and calcium depletion. The lowest concentrations of H2O2 (0.5 and 0.1 mM)-induced delayed cytotoxicity (at 24 or 48 hr), which was not associated with DNA ladder formation or morphologic evidence of apoptosis, but was inhibited by ABA. Enforced expression of BCL-2 induced resistance to 0.5 and 0.1 mM H2O2 but had no effect on cytotoxicity induced by 5 and 10 mM. Exposure of isolated nuclei to H2O2 in the absence of calcium or magnesium failed to induce endonucleosomal fragmentation. These data indicate that distinct pathways of H2O2-induced cytotoxicity can be distinguished by their different concentration dependences, and that BCL-2 can protect against some forms of H2O2-induced cytotoxicity.

Atypical apoptotic cell death induced in L929 targets by exposure to tumor necrosis factor.

The mechanism by which tumor necrosis factor (TNF) induces cytotoxicity of murine fibroblasts was investigated. Electrophoresis of DNA extracted from TNF-treated L929 targets showed fragmentation of DNA into a ladder-like pattern, typical of cells dying by apoptosis. Morphologic analysis also indicated apoptotic cell death, demonstrating clumping and crescentic condensation of chromatin. In contrast, chromatin condensation and ladder-like DNA fragmentation were not detected in L929 targets dying by necrosis from exposure to heat, repeated cycles of freeze-thaw, and sodium azide. Chromatin condensation was an early event, detected as early as 6 h of incubation. However, DNA fragmentation (assayed by double-stranded fragmentation assay and gel electrophoresis), as well as the apoptotic changes detected by Hoechst fluorescence, both occurred later and did not precede TNF cytotoxicity (membrane permeabilization detected by trypan blue or propidium iodide staining). This atypical pattern of apoptosis was a characteristic of L929 target cells rather than a generalized cytotoxic response to TNF because TNF-treated squamous cancer cells showed typical features of apoptosis (DNA fragmentation before cytotoxicity) and etoposide-treated L929 cells demonstrated the same atypical kinetics as TNF-treated cells. Zinc significantly inhibited TNF cytotoxicity as well as DNA fragmentation of L929. However, because DNA fragmentation occurred belatedly in TNF-treated targets, lagging behind cytotoxicity, the protection by zinc against TNF appears mediated by events that occur before the ultimate endonuclease-induced cleavage of DNA into small fragments.

Inhibition of DNA repair with aphidicolin enhances sensitivity of targets to tumor necrosis factor.

To test whether DNA injury contributes to TNF-induced cytotoxicity, we attempted to enhance DNA injury by inhibiting its repair and then assessing effects on cytotoxicity. DNA repair, assayed as unscheduled DNA synthesis, was first detected in TNF-sensitive targets by 2-3 h of incubation with TNF. Targets resistant to TNF cytotoxicity did not demonstrate significant repair replication. Repair preceded the detection of TNF-induced DNA injury, which was subsequently demonstrated by a double-stranded DNA fragmentation assay, sedimentation of DNA in neutral and alkaline sucrose gradients, and gel electrophoresis of extracted DNA. This suggested that early during exposure to TNF, DNA repair proceeds more rapidly than strand breakage. To inhibit repair, nontoxic concentrations of aphidicolin (inhibitor of DNA polymerase-alpha) and dideoxythymidine (inhibitor of DNA polymerase-beta and gamma) were used. Aphidicolin inhibited repair and consistently sensitized to TNF cytotoxicity, decreasing the ID50 for TNF at least 10- to 50-fold. In contrast, dideoxythymidine had no effect on repair or cytotoxicity. Deoxycytidine, which competitively inhibits binding of aphidicolin to DNA polymerase, blocked the sensitization in a concentration-dependent fashion. In targets sensitized with aphidicolin, TNF-induced strand breakage was accelerated, being detected by 4 h of culture in the sucrose gradient assay. Sensitization to TNF was not due to a heightened activation of poly (ADP-ribose) polymerase. These results indicate that TNF-induced strand breakage participates in TNF-induced cytotoxicity and that the level of DNA repair plays a role in determining relative sensitivity of targets.

Effect of Diethylpyrocarbonate on the Allosteric Properties of Phosphoenolpyruvate Carboxylase from Crassula argentea.

Phosphoenolpyruvate carboxylase from the Crassulacean acid metabolism plant Crassula argentea was substantially desensitized to the effects of regulatory ligands by treatment with diethylpyrocarbonate, a reagent which selectively modifies histidyl residues. Desensitization of the enzyme to the inhibitor malate and the activator glucose 6-phosphate was accompanied by the appearance of a peak in the ultraviolet difference spectrum at 240 nanometers, indicating the formation of ethoxyformylhistidyl derivatives. Hydroxylamine reversed part of the spectral change under native conditions, and almost all of the change under denaturing conditions, but failed to restore sensitivity to effectors. The pH profiles of desensitization to malate and glucose 6-phosphate indicated the involvement of groups on the enzyme with pK, values of 6.8 and 6.4, respectively. Under denaturing conditions, a total of 15 histidine residues per subunit were modified by diethylpyrocarbonate, whereas for the native enzyme nine histidines were modified per subunit. Effector desensitization occurs after the modification of two to three histidyl residues per subunit. The presence of malate reduced the apparent rate constant for desensitization by 60%, suggesting that the modification occurred at the malate binding site. Diethylpyrocarbonate treatment also eliminated the kinetic lag caused by malate. Glucose 6-phosphate did not protect the enzyme against diethylpyrocarbonate-induced desensitization.

The "Sulfamylon sandwich"--a laminated mafenide-saline dressing.

Though commercially available 11.2% mafenide acetate cream (Sulfamylon) has been shown to be very effective in preventing burn wound sepsis, it has several serious drawbacks. Five percent mafenide acetate solution dressings are also effective and do not have the disadvantages of the cream. This preparation, however, is not available for general usage. For these reasons, we have devised a laminated dressing using the 11.2% cream and saline, which delivers an aqueous solution of mafenide acetate to the wound. The dressing has proved both effective and acceptable to patients, and is particularly valuable following the application of split-thickness skin grafts to burns and other chronic open wounds. The technique is described.