No abstract available.
Toxoplasma* ; Toxoplasmosis*

PURPOSE: Heat shock protein (HSP) 27 protects the cell by controlling apoptosis and immune reactions, and c-FLIP (cellular-FLICE inhibitory protein) inhibits apoptosis by inhibiting caspase-8 activity. We investigated the relationship of HSP27 and c-FLIP expression to prostate-specific antigen, Gleason score sum (GSS), and pathologic stage. MATERIALS AND METHODS: Samples from 163 patients between May 2004 and April 2010 were analyzed: 83 from patients that had underwent a radical prostatectomy, and 80 from those that underwent transurethral resection of the prostate to alleviate urinary symptoms from benign prostate hyperplasia. c-FLIP and HSP27 expression were observed by immunohistochemistry staining. Samples with less than 5% expression-positive cells were scored as 1, with 5%-50% were scored as 2, and with more than 50% were scored as 3. Local reactions were identified as 0.5 and evaluated. RESULTS: Both the presence of HSP27 within the tumor and the number of cancer cells positive for HSP27 were significantly correlated to GSS and pathologic stage (p<0.001, p=0.001, p<0.001, p<0.001). The same was true for c-FLIP expression (p<0.001). GSS was more highly correlated to HSP27 expression than to c-FLIP expression (r=0.814 for HSP27, r=0.776 for c-FLIP), as was pathologic stage (r=0.592 for HSP27, r=0.554 for c-FLIP). CONCLUSIONS: In prostate cancer, higher GSS and a more advanced pathologic stage were associated with a higher likelihood of having a HSP27-positive tumor and more HSP27-positive tumor cells. HSP27 expression was correlated with GSS and prostate cancer stage. A more advanced pathologic stage corresponded to a higher likelihood of having a c-FLIP-positive tumor and more c-FLIP-positive tumor cells. HSP27 expression had a higher correlation with prostate cancer stage and GSS than c-FLIP expression did.
Aged ; Biomarkers, Tumor/*metabolism ; CASP8 and FADD-Like Apoptosis Regulating Protein/*metabolism ; HSP27 Heat-Shock Proteins/*metabolism ; Humans ; Lymphatic Metastasis ; Male ; Middle Aged ; Neoplasm Grading ; Neoplasm Proteins/metabolism ; Neoplasm Staging ; Prostatectomy/methods ; Prostatic Hyperplasia/metabolism/surgery ; Prostatic Neoplasms/*metabolism/pathology/surgery ; Transurethral Resection of Prostate

BACKGROUND: Heat-treated cells are known to be protected from lysis by TNF, which is considered to play a central role in the pathogenesis of sepsis-induced acute lung injury. The objective of the study was to investigate the effect of heat shock response by heat-pretreatment on the acute lung injury of the rats induced by intratracheally administered TNF-alpha. METHODS: We intratracheally instilled either saline or TNF (R&D, 500ng) with and without heat pretreatment in Sprague-Dawley rats weighing 250-350 g. The heated rats were raised their rectal temperature to 41degrees C and was maintained thereafter for 13 minutes at 18 h before intratracheal administration of saline or TNF. After 5 h of intratracheal treatment, lung leak, lung myeloperoxidase activity (MPO) and heat shock proteins were measured in rats. Lung leak index was defined as counts per minute of I125 in the right lung divided by counts per minutes of I125 in 1.0 ml of blood. All data are expressed as means+/-SE. RESULTS: There is no difference in acute lung leak index (0.099+/-0.024 vs 0.123+/-0.005) among the rats given saline intratracheally with and without heat pretreatment, but MPO activity showed a decreased tendency in heat-pretreated rats (4.58+/-0.79 U/g) compared with heat-unpretreated rats (7.32+/-0.97 U/g) (P= 0.064). Rats administered TNF intratracheally with heat-pretreatment had decreased lung leak index (0.137+/-0.012) and lung MPO activity (5.51+/-1.04 U/g) compared with those of heat-unpretreated and TNF-administered rats (0.186+/-0.016, 14.34+/-1.22 U/g) (P<0.05 in each). There were no significant difference of lung leak index and MPO activity between TNF-treated rats with heat-pretreatment and saline-treated rats with and without heat-pretreatment CONCLUISON: The heat shock response attenuated neutrophil recruitment and acute lung leak induced by intratracheal instillation of TNF-in rats.
Acute Lung Injury* ; Animals ; Heat-Shock Proteins ; Heat-Shock Response* ; Hot Temperature* ; HSP70 Heat-Shock Proteins ; Lung ; Necrosis* ; Neutrophil Infiltration ; Neutrophils ; Peroxidase ; Rats* ; Rats, Sprague-Dawley ; Respiratory Distress Syndrome, Adult ; Tumor Necrosis Factor-alpha