Toxoplasma gondi Inhibits Apoptosis in Infected Cells by Caspase Inactivation and NF-kappaB Activation

Our experiments aimed to clarify the mechanism by which host cell apoptosis is inhibited by infection with the intracellular protozoan parasite, Toxoplasma gondii (T. gondii). Mouse spleen cells were cultured in 6-well plates with RPMI 1640/ 10% FBS at 37(i)E, in a 5% CO2 atmosphere. Apoptosis of spleen cells was induced by actinomycin-D (AD) treatment for 1 h prior to infection with T. gondii. A variety of assays were used to assess the progression of apoptosis: DNA size analysis on agarose gel electrophoresis, flow cytometry with annexin V/PI staining, and analysis of expression levels of Bcl-2 family and NF-kappaB mRNA and proteins by RT-PCR, Western blotting, and EMSA. Additionally, transmission electron microscopy (TEM) was performed to observe changes in cell morphology. Fragmentation of DNA was inhibited in spleen cells treated with AD and T. gondii 5 h and 18 h post infection, respectively, and flow cytometry studies showed a decreased apoptotic rates in AD and T. gondii treated spleen cells. We observed decreased expression of Bax mRNA and protein, while levels of Bcl-2 mRNA remained constant in spleen cells treated with AD and T. gondii. Caspase 3 and PARP were inactivated in cells treated with AD and T. gondii, and increased levels of cleaved caspase 8 were also observed. Analysis of EMSA and Western blot data suggests that activation of transcription factor NF-kappaB may be involved in the blockade of apoptosis by T. gondii. TEM analysis showed nuclear fragmentation and chromatin condensation occurring in spleen cells treated with AD; however, such apoptosis- associated morphological changes were not observed in cells treated with both AD and T. gondii tachyzoites. Together, these data show that T. gondii infection inhibits AD induced apoptosis via caspase inactivation and NF-kappaB activation in mouse spleen cells.

Toxoplasma gondi Inhibits Apoptosis in Infected Cells by Caspase Inactivation and NF-kappaB Activation

Our experiments aimed to clarify the mechanism by which host cell apoptosis is inhibited by infection with the intracellular protozoan parasite, Toxoplasma gondii (T. gondii). Mouse spleen cells were cultured in 6-well plates with RPMI 1640/ 10% FBS at 37(i)E, in a 5% CO2 atmosphere. Apoptosis of spleen cells was induced by actinomycin-D (AD) treatment for 1 h prior to infection with T. gondii. A variety of assays were used to assess the progression of apoptosis: DNA size analysis on agarose gel electrophoresis, flow cytometry with annexin V/PI staining, and analysis of expression levels of Bcl-2 family and NF-kappaB mRNA and proteins by RT-PCR, Western blotting, and EMSA. Additionally, transmission electron microscopy (TEM) was performed to observe changes in cell morphology. Fragmentation of DNA was inhibited in spleen cells treated with AD and T. gondii 5 h and 18 h post infection, respectively, and flow cytometry studies showed a decreased apoptotic rates in AD and T. gondii treated spleen cells. We observed decreased expression of Bax mRNA and protein, while levels of Bcl-2 mRNA remained constant in spleen cells treated with AD and T. gondii. Caspase 3 and PARP were inactivated in cells treated with AD and T. gondii, and increased levels of cleaved caspase 8 were also observed. Analysis of EMSA and Western blot data suggests that activation of transcription factor NF-kappaB may be involved in the blockade of apoptosis by T. gondii. TEM analysis showed nuclear fragmentation and chromatin condensation occurring in spleen cells treated with AD; however, such apoptosis- associated morphological changes were not observed in cells treated with both AD and T. gondii tachyzoites. Together, these data show that T. gondii infection inhibits AD induced apoptosis via caspase inactivation and NF-kappaB activation in mouse spleen cells.

APACHE II Score and Multiple Organ Failure Score as Predictors of Mortality Rate of Critically Ill Patients / 대한마취과학회지

BACKGROUND: The APACHE II scoring system has been regarded as a useful tool in the assessment of the severity of injury and prognosis for acutely ill patients. Recently, there have been many reports that multiple organ failure(MOF) score is the better predictor of the mortality of critically ill patients than any other scoring system. The purpose of this study was to compare APACHE II score and MOF score for mortality prediction in critically ill patients. METHODS: 163 critically ill patients were studied. We analyzed the correlation between the mortality rate and the scores that were produced by APACHE II and MOF scoring system within the first 24 hours in the ICU. We analyzed the correlation between each score and the number of days of ICU stay. We also calculated the mortality rate according to the number of organ failure. RESULTS: 1) The APACHE II score and MOF score of the survivors(n=129) were 9 6 and 1 1, respectively and those of nonsurvivors(n=34) were 16 7 and 5 2(mean SD), respectively. 2) The r2 was 0.62 between APACHE II score and mortality rate, and 0.77 between MOF score and mortality rate. 3) The r2 was 0.06 between APACHE II score and ICU stay, 0.01 between MOF score and ICU stay. 4) The mortality rates were 0, 2, 20, 64, 73, 75 and 100 % in 0, 1, 2, 3, 4, 5 and 6 organ failures, respectively. CONCLUSIONS: The MOF score was more sensitive predictor of the mortality of critically ill patients than the APACHE II score.

Comparison of Anesthesiology Related Terminology in Korea, China and Japan / 대한마취과학회지

BACKGROUND: The purpose of this study is followings: First, to find out similarity in anesthesiology related terminology in Korea, China and Japan. Second, to clarify the use of Chinese character in making anesthetic terminology in Korea. Third, in attempt to explore the criteria in making terminology. METHODS: 335 terms were selected in anesthetic terminology book and allocated to English term. RESULTS: 44 terms(13%) were same in Chinese character among three countries, 144 terms(43%) were different in each other, 141 terms (42%) were same between two countries (Korea-China 9, Korea-Japan 130 and China-Japan 2). CONCLUSIONS: Only small terms were same in three countries and nearly half of terms were different. Most of same terms in two countries came from Korea-Japan. It seemed that three countries had their own terms in anesthesiology. Making terminology with Chinese character were not believed to be the best and only way. Moreover, it was suspicious using Chinese character as communicating tool among three countries. Creative efforts with our own native language for better terminology in this field were expected.

Intracellular Mechanism of Sevoflurane`s Effect on Isolated Vascular Rings of the Rabbits / 대한마취과학회지

The purpose of this study were to elucidate how sevoflurane affects vascular smooth musde and to understand the intracellular mechanism of sevoflurane. Isolated aortic rings of the rabbit were examined. Rings were mounted on tissue bath containing 40 ml of modified Krebs solution bubbled with 95% O2/5% CO2 and attached to force transducers. The preparations were contracted with either 40 mM KC1, or 0.1 uM norepinephrine followed by 0.1 uM acetylcholine (and 1 nM ryanodine)- or 2.8 mM lidocaine induced relaxation. At steady state contraction or relaxation, the effects of sevoflurane (2, 4, 5%) were studied. The steady state tension before administration of sevoflurane was considered as 100% and the changing tension during sevoflurane was expressed as a percentage. Sevoflurane (2, 4, 5%) produced relaxing effects (99.4+/-0.6, 98.1+/-0.9, 95.9+/-1.0%) on KC1-induced tension, independent of endothelium. Sevoflurane increased tension in the acetylcholine (55.4+/-5.1%)- or lidocaine (75.3+/-8.3%)- relaxed state (acetylcholine: 73.6+/-5.3, 86.8+/-3.2, 94.1+/-5.2%, acetylcholine+ryanodine ; 63.7+/-4.6, 68.6+/-7.2, 70.4+/-2.5%, lidocaine ; 83.7+/-7.0, 84.6+/-12.1, 85.3+/-4.4%). The effects were dose-dependent manner. It is concluded that sevoflurane directly alters vascular contraction or relaxation in relation to Ca2+ mobilization on condition and that mechanism of sevofluranes effects on the sarcoplasmic reticulum may play a primary role.