Botryomycosis mimicking acute abdome: a case report

Botryomycosis is a rare chronic granulomatous bacterial infection involving mostly the skin and subcutaneous tissues. The nomenclature is a misnomer as it is caused by true bacteria and not by fungus. This uncommon infection sometimes simulates neoplasia and actinomycosis. Staphylococcus aureus is the agent isolated in most cases, followed by Pseudomonas sp. cepas. The authors present an uncommon case of invasive umbilical Botriomycosis simulating an acute abdome. A combination of surgery and antibiotic therapy treatment was applied with complete resolution of the infection. More often seen in the skin, this is the first report of Botryomycosis affecting this site

Combined effects of melatonin and topical hypothermia on renal ischemia-reperfusion injury in rats

Purpose: To evaluate whether their combination was more effective than either alone in decreasing renal damage due to ischemia/reperfusion (I/R) injury in rats. Methods: Thirty-two Wistar rats were assigned to four groups. Following right nephrectomy, their left kidneys were subjected to warm ischemia (IR), cold ischemia (TH+IR), intraperitoneal injection of 10 mg/kg melatonin (MEL+IR), or injection of 10 mg/kg melatonin followed by cold ischemia (MEL+TH+IR). Eight randomly assigned right kidneys constituted the control group. After 240 min of reperfusion, left nephrectomy was performed for histopathological evaluation, lipid peroxidation, and measurement of antioxidant enzyme activity. Serum was collected to measure urea and creatinine concentrations. Results: Histopathological damage induced by ischemia and reperfusion was more attenuated in the MEL+TH+IR group than in the MEL+IR and TH+IR groups (p<0.037). Superoxide dismutase activity was significantly higher (p<0.029) and creatinine (p<0.001) and urea (p<0.001) concentrations were significantly lower in the MEL+TH+IR group than in the MEL+IR and TH+IR groups. Conclusion: The combination of melatonin (MEL) and topical hypothermia (TH) better protects against renal I/R injury than does MEL or TH alone

Induction of selective liver hypothermia prevents significant ischemia/reperfusion injury in Wistar rats after 24 hours

Purpose: To investigate the effects of induction of selective liver hypothermia in a rodent model. Methods: Seven male Wistar rats were subjected to 90 minutes of partial 70% liver ischemia and topic liver 26°C hypothermia (H group). Other seven male Wistar rats were subjected to 90 minutes of partial 70% normothermic liver ischemia (N group). Five additional rats underwent a midline incision and section of liver ligaments under normothermic conditions and without any liver ischemia (sham group). All animals were sacrificed 24-h after reperfusion, and livers were sampled for analyses. Pathology sections were scored for sinusoidal congestion, ballooning, hepatocelllular necrosis and the presence of neutrophilic infiltrates. Results: At the end of the experiment, liver tissue expressions of TNF-ɑ, IL-1β, iNOS and TNF-ɑ/IL-10 ratio were significantly reduced in the H group compared to N group, whereas IL-10 and eNOS were significantly increased in H group. Histopathological injury scores revealed a significant decrease in ischemia/reperfusion (I/R) injuries in H group. Conclusion: Selective liver hypothermia prevented I/R injury by inhibiting the release of inflammatory cytokines, preserves microcirculation, prevents hepatocellular necrosis and leukocyte infiltration, allowing maintenance of the liver architecture

Botryomycosis mimicking acute abdome: a case report

Botryomycosis is a rare chronic granulomatous bacterial infection involving mostly the skin and subcutaneous tissues. The nomenclature is a misnomer as it is caused by true bacteria and not by fungus. This uncommon infection sometimes simulates neoplasia and actinomycosis. Staphylococcus aureus is the agent isolated in most cases, followed by Pseudomonas sp. cepas. The authors present an uncommon case of invasive umbilical Botriomycosis simulating an acute abdome. A combination of surgery and antibiotic therapy treatment was applied with complete resolution of the infection. More often seen in the skin, this is the first report of Botryomycosis affecting this site

Oxidative stress evaluation of ischemia and reperfusion in kidneys under various degrees of hypothermia in rats

PURPOSE: To design an animal model of ischemia-reperfusion (I/R) in kidneys and evaluate the role that predetermined ranges of local hypothermia plays on markers of stress-oxydative as well as on histologic sections. METHODS: Twenty eight male rats Wistar, under general anesthesia, undergone right nephrectomy (G0, control group) followed by left kidney ischemia during 40 min. Four temperatures groups were designed, with seven animals randomized for each group: normothermic (G1, ±37oC), mild hypothermia (G2, 26oC), moderate hypothermia (G3, 15oC) and deep hypothermia (G4, 4oC). Left kidney temperature was assessed with an intraparenchymal probe. Left nephrectomy was performed after 240 min of reperfusion. After I/R a blood sample was obtained for f2-IP. Half of each kidney was sent to pathological evaluation and half to analyze CAT, SOD, TBARS, NO3, NO2. RESULTS: Histopathology showed that all kidneys under I/R were significantly more injured than the G0 (p<0.001). TBARS had increased levels in all I/R groups compared with the G0 (p<0.001). CAT had a significant difference (p<0.03) between G1 and G4. Finally, no difference was found on SOD, NO3, NO2 nor on f2-IP. CONCLUSION: This model of I/R was efficient to produce oxidative-stress in the kidney, showing that 4ºC offered significant decrease in free radicals production, although tissue protection was not observed

Oxidative stress evaluation in ischemia and reperfusion in kidneys underwent to variation of local temperature in an animal model

Introdução: embora a lesão por isquemia e reperfusão (I/R) renal possa ser reduzida por resfriamento, nenhuma análise sistemática in vivo da influência da temperatura foi empregada até o momento para avaliar o efeito de diferentes temperaturas nos danos provocados pela I/R renal. Objetivos: desenvolver um modelo experimental em ratos para avaliar os efeitos da variação local de temperatura (hipotermia renal tópica) nos danos, ou na prevenção destes, provocados por I/R. Além do desenvolvimento do modelo experimental, outro objetivo foi medir o efeito do estresse-oxidativo em diferentes grupos de temperatura no modelo experimental desenvolvido por nós. Métodos: estudo randomizado com ratos Wistar, machos adultos, pesando cerca de 400g, foram randomizados para quatro grupos experimentais com 7 animais em cada grupo. No grupo 1 a temperatura renal tópica foi ambiental; no grupo 2 foi induzida hipotermia local leve (26ºC) através do gotejamento de solução fisiológica resfriada até o alcance da temperatura-alvo; no grupo 3 a hipotermia tópica foi moderada (15ºC); e no grupo 4 a hipotermia profunda (4ºC) foi atingida através da utilização de solução fisiológica congelada (gelo). A temperatura sistêmica foi medida por termômetro retal. Já a temperatura cortical renal foi medida por termômetro com sonda intraparenquimatosa. Após anestesia geral através de injeção intraperitoneal de Ketamina (75mg/Kg) e Xilazina (10mg/Kg), os ratos foram submetidos a canulação retrorbital para obtenção de amostra de sangue antes da laparotomia. A seguir procedeu-se com nefrectomia direita (rim controle, removido logo após a laparotomia e não submetido a I/R ou hipotermia). O rim esquerdo teve interrupção do fluxo arterial ao longo de 40 minutos (isquemia). De acordo com o grupo, o rim era ou não resfriado. O resfriamento era mantido na temperatura alvo até o término dos 40 minutos. O rim era então reperfundido e o abdome era suturado. Os animais permaneciam em gaiola aquecida com água a disposição, mas não alimentos. Após 240 minutos de reperfusão os animais eram reoperados sob nova anestesia geral. O rim esquerdo e o sangue eram coletados, e os ratos eram sacrificados. O rim direito foi considerado o grupo controle, assim como o sangue coletado antes da laparotomia. A avaliação dos desfechos incluiu a medida de catalase (CAT), de superóxido dismutase (SOD), de ácido tiobarbicúrico (TBARS), de nitritos (NO2) e de nitratos (NO3) teciduais, além da medida de F2-isoprostanos (F2IP) plasmáticos. Também foi realizado exame histopatológico renal em hematoxilina-eosina (HE). Resultados: o exame histopatológico revelou que I/R (40’/240’) provocou lesão renal, independentemente da temperatura cortical renal, quando comparado com o grupo controle (P < 0,001). TBARS, um dos produtos da peroxidação lipídica, mostrou aumento em todos os grupos submetidos a I/R, independentemente da temperatura, em relação ao grupo controle. Catalase, enzima protetora contra o estresse oxidativo, mostrou aumento no grupo I/R normotérmico (G1, 37ºC) quando comparado ao grupo controle, indicando mobilização celular de mecanismos protetores intrínsecos. À medida que a temperatura era diminuída no grupo I/R, ocorreu diminuição da catalase em relação ao controle, mas sobretudo em relação ao I/R normotérmico, indicando que a hipotermia foi um mecanismo extrínseco de proteção, dispensando a mobilização da catalase. Foi detectada uma diferença estatisticamente significativa entre o grupo I/R normotérmico (G1, 37ºC) e o grupo submetido à hipotermia profunda (G4, 4ºC), com um P < 0.03. A avaliação dos demais marcadores de desfecho não mostrou diferenças estatisticamente significativas. Conclusões: isquemia renal de 40 minutos seguida de reperfusão por 240 minutos provocou lesão renal com alterações histopatológicas e também em um marcador de estresse oxidativo (TBARS). A avaliação da catalase (CAT) demonstrou que a hipotermia profunda (4ºC) foi provavelmente protetora, embora não tenha havido tradução histopatológica dessa proteção, nesse experimento agudo (240 minutos de reperfusão pós-isquêmica).Introduction: Hypothermia has been associated with prevention against ischemiareperfusion (I/R) damage, but there is no experimental analysis, in vivo, regarding the role that hypothermia plays on renal injury induced by I/R. Objectives: The aims of this study were to design an animal model and evaluate the impact of predetermined ranges of temperatures on markers of oxidative stress and renal histologic sections. Methods: 28 Wistar male rats, under general anesthesia, undergone laparatomy to collect the right kidney (control group in each animal). The vascular pedicle of the left kidney was clamped during 40 minutes (ischemia). Four temperatures groups were designed, with 7 animals randomized for each group: normothermic (around 37oC), mild local hypothermia (26oC), moderate local hypothermia (15oC) and deep hypothermia (4oC). The systemic body temperature was kept during the operation through the warming of the surgical table. The left kidney cortical temperature was assessed with an intra parenchymal probe connected to a thermometer. For the systemic temperature measurement it was applied a common electronic rectal thermometer. After 40 minutes of ischemia, the left kidney had the vascular clamp removed, and the abdominal wall had been closed in two layers. The animals were kept alive in an incubator for 240 minutes, so they were re-laparotomized, under new anesthesia, and the left kidney was removed. Afterwards it was performed heart puncture in order to collect blood sample for plasmatic f2-isoprostanes. Half of each kidney (right and left, of all animals) had been kept on formalin and sent to pathological evaluation. The tissues stored on the freezer were used to analyze oxidative stress markers: catalase, SOD, TBARS, NO3, and NO2. Results: Core body temperature had not differed significantly between the groups. According to the pathological evaluation, all kidneys that suffered ischemia were significantly more injured than the controls (p < 0.001). No injury was found on the control group (right kidney of each rat). TBARS showed quite similar findings, showing increased levels in all I/R groups compared with the control group (P < 0.001). Concerning the protective enzyme catalase, it was observed an increase of this enzyme on the ischemic normothermic kidney when compared to the control. As the temperature was decreasing, more the catalase was decreasing, reaching a significant statistical difference (P < 0.03) between the ischemic normothermic group (G1, 37ºC) and the deepest hypothermic group (G4, 4ºC). No difference was found on nitrites and nitrates, superoxide dismutase, or on the plasmatic isoprostanes. Conclusion: This model was efficient in produce oxidative stress by I/R. Deep hypothermia has offered protection in this acute experiment (40 min of ischemia followed by 240 min of reperfusion)

Desenvolvimento de técnica para avaliação da atividade das isoenzimas 5-alfa-redutase I e II em tecido prostático de pacientes do Hospital de Clínicas de Porto Alegre

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Oxidative stress evaluation in ischemia and reperfusion in kidneys underwent to variation of local temperature in an animal model

Introdução: embora a lesão por isquemia e reperfusão (I/R) renal possa ser reduzida por resfriamento, nenhuma análise sistemática in vivo da influência da temperatura foi empregada até o momento para avaliar o efeito de diferentes temperaturas nos danos provocados pela I/R renal. Objetivos: desenvolver um modelo experimental em ratos para avaliar os efeitos da variação local de temperatura (hipotermia renal tópica) nos danos, ou na prevenção destes, provocados por I/R. Além do desenvolvimento do modelo experimental, outro objetivo foi medir o efeito do estresse-oxidativo em diferentes grupos de temperatura no modelo experimental desenvolvido por nós. Métodos: estudo randomizado com ratos Wistar, machos adultos, pesando cerca de 400g, foram randomizados para quatro grupos experimentais com 7 animais em cada grupo. No grupo 1 a temperatura renal tópica foi ambiental; no grupo 2 foi induzida hipotermia local leve (26ºC) através do gotejamento de solução fisiológica resfriada até o alcance da temperatura-alvo; no grupo 3 a hipotermia tópica foi moderada (15ºC); e no grupo 4 a hipotermia profunda (4ºC) foi atingida através da utilização de solução fisiológica congelada (gelo). A temperatura sistêmica foi medida por termômetro retal. Já a temperatura cortical renal foi medida por termômetro com sonda intraparenquimatosa. Após anestesia geral através de injeção intraperitoneal de Ketamina (75mg/Kg) e Xilazina (10mg/Kg), os ratos foram submetidos a canulação retrorbital para obtenção de amostra de sangue antes da laparotomia. A seguir procedeu-se com nefrectomia direita (rim controle, removido logo após a laparotomia e não submetido a I/R ou hipotermia). O rim esquerdo teve interrupção do fluxo arterial ao longo de 40 minutos (isquemia). De acordo com o grupo, o rim era ou não resfriado. O resfriamento era mantido na temperatura alvo até o término dos 40 minutos. O rim era então reperfundido e o abdome era suturado. Os animais permaneciam em gaiola aquecida com água a disposição, mas não alimentos. Após 240 minutos de reperfusão os animais eram reoperados sob nova anestesia geral. O rim esquerdo e o sangue eram coletados, e os ratos eram sacrificados. O rim direito foi considerado o grupo controle, assim como o sangue coletado antes da laparotomia. A avaliação dos desfechos incluiu a medida de catalase (CAT), de superóxido dismutase (SOD), de ácido tiobarbicúrico (TBARS), de nitritos (NO2) e de nitratos (NO3) teciduais, além da medida de F2-isoprostanos (F2IP) plasmáticos. Também foi realizado exame histopatológico renal em hematoxilina-eosina (HE). Resultados: o exame histopatológico revelou que I/R (40’/240’) provocou lesão renal, independentemente da temperatura cortical renal, quando comparado com o grupo controle (P < 0,001). TBARS, um dos produtos da peroxidação lipídica, mostrou aumento em todos os grupos submetidos a I/R, independentemente da temperatura, em relação ao grupo controle. Catalase, enzima protetora contra o estresse oxidativo, mostrou aumento no grupo I/R normotérmico (G1, 37ºC) quando comparado ao grupo controle, indicando mobilização celular de mecanismos protetores intrínsecos. À medida que a temperatura era diminuída no grupo I/R, ocorreu diminuição da catalase em relação ao controle, mas sobretudo em relação ao I/R normotérmico, indicando que a hipotermia foi um mecanismo extrínseco de proteção, dispensando a mobilização da catalase. Foi detectada uma diferença estatisticamente significativa entre o grupo I/R normotérmico (G1, 37ºC) e o grupo submetido à hipotermia profunda (G4, 4ºC), com um P < 0.03. A avaliação dos demais marcadores de desfecho não mostrou diferenças estatisticamente significativas. Conclusões: isquemia renal de 40 minutos seguida de reperfusão por 240 minutos provocou lesão renal com alterações histopatológicas e também em um marcador de estresse oxidativo (TBARS). A avaliação da catalase (CAT) demonstrou que a hipotermia profunda (4ºC) foi provavelmente protetora, embora não tenha havido tradução histopatológica dessa proteção, nesse experimento agudo (240 minutos de reperfusão pós-isquêmica).Introduction: Hypothermia has been associated with prevention against ischemiareperfusion (I/R) damage, but there is no experimental analysis, in vivo, regarding the role that hypothermia plays on renal injury induced by I/R. Objectives: The aims of this study were to design an animal model and evaluate the impact of predetermined ranges of temperatures on markers of oxidative stress and renal histologic sections. Methods: 28 Wistar male rats, under general anesthesia, undergone laparatomy to collect the right kidney (control group in each animal). The vascular pedicle of the left kidney was clamped during 40 minutes (ischemia). Four temperatures groups were designed, with 7 animals randomized for each group: normothermic (around 37oC), mild local hypothermia (26oC), moderate local hypothermia (15oC) and deep hypothermia (4oC). The systemic body temperature was kept during the operation through the warming of the surgical table. The left kidney cortical temperature was assessed with an intra parenchymal probe connected to a thermometer. For the systemic temperature measurement it was applied a common electronic rectal thermometer. After 40 minutes of ischemia, the left kidney had the vascular clamp removed, and the abdominal wall had been closed in two layers. The animals were kept alive in an incubator for 240 minutes, so they were re-laparotomized, under new anesthesia, and the left kidney was removed. Afterwards it was performed heart puncture in order to collect blood sample for plasmatic f2-isoprostanes. Half of each kidney (right and left, of all animals) had been kept on formalin and sent to pathological evaluation. The tissues stored on the freezer were used to analyze oxidative stress markers: catalase, SOD, TBARS, NO3, and NO2. Results: Core body temperature had not differed significantly between the groups. According to the pathological evaluation, all kidneys that suffered ischemia were significantly more injured than the controls (p < 0.001). No injury was found on the control group (right kidney of each rat). TBARS showed quite similar findings, showing increased levels in all I/R groups compared with the control group (P < 0.001). Concerning the protective enzyme catalase, it was observed an increase of this enzyme on the ischemic normothermic kidney when compared to the control. As the temperature was decreasing, more the catalase was decreasing, reaching a significant statistical difference (P < 0.03) between the ischemic normothermic group (G1, 37ºC) and the deepest hypothermic group (G4, 4ºC). No difference was found on nitrites and nitrates, superoxide dismutase, or on the plasmatic isoprostanes. Conclusion: This model was efficient in produce oxidative stress by I/R. Deep hypothermia has offered protection in this acute experiment (40 min of ischemia followed by 240 min of reperfusion)