Liver perfusion CT during hepatic arteriography for the hepatocellular carcinoma: dose reduction and quantitative evaluation for normal- and ultralow-dose protocol.

OBJECTIVES: The purpose of this study was to investigate whether substantial reduction of the computed tomography (CT) dose is possible in liver CT perfusion imaging by comparing the results of ultralow-dose CT perfusion imaging with those of conventional CT perfusion imaging the same patients and under the same conditions. MATERIALS AND METHODS: The study was composed following two parts: computer simulation and patients study. In computer simulation, noise was added to the images so that the standard deviation (SD) of the CT values in the liver parenchyma became various values using ImageJ. Time density curves (TDCs) were created from the simulated data, and the influence of difference in the SDs on the shapes of the TDCs was investigated. In the patient study, CT perfusion during intra-arterial injection was performed in 30 consecutive patients undergoing transcatheter arterial chemoembolization. CT perfusion images were acquired twice, at 100 mA (CTDI(vol), 300 mGy) for normal and at 20 mA (CTDI(vol), 60 mGy) for the ultralow radiation doses, under the same conditions. RESULTS: No change was observed in the shape of the TDCs and peak values in the analysis of simulation images. A very good correlation was observed between the normal- and ultralow-dose CT images for all analyzed values (R(2)=0.9885 for blood flow, 0.9269 for blood volume, and 0.8424 for mean transit time). CONCLUSIONS: Our results demonstrated that there was no significant difference in the analysis results of perfusion CT between ultralow-dose CT performed using 20% of the conventional dose and normal-dose CT perfusion.

High mobility group box 1 is upregulated after spinal cord injury and is associated with neuronal cell apoptosis.

STUDY DESIGN: Cerebrocortical culture and rat spinal cord injury (SCI) model were used to examine the expression of high mobility group box 1 (HMGB1), TNF-alpha, and Rage by reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemical examination. In addition, relationship between upregulation of HMGB1 and neural cells apoptosis was evaluated after SCI. OBJECTIVE: To evaluate the upregulation of HMGB1, TNF-alpha, and Rage after SCI. SUMMARY OF BACKGROUND DATA: It is known that the mode of delayed neuronal cell death after SCI is apoptosis. Apoptotic cell death is influenced by several injury-promoting factors which include pro-inflammatory cytokines. Inhibition of apoptosis promotes neurologic improvement following SCI. However, the factors which transmit inflammatory signaling following SCI have not yet been clarified in detail. HMGB1 was reported as an important mediator of inflammation. We examined the expression of HMGB1, TNF-alpha and Rage following acute SCI. METHODS: Expression of HMGB1, TNF-alpha and Rage was examined by RT-PCR and immunohistochemical examination. Apoptotic cell death was evaluated by TUNEL methods. RESULTS: HMGB1 was exported from nuclei to cytoplasm in active caspase-3 positive apoptotic cell in vitro. In addition, HMGB1, TNF-alpha, and Rage was expressed in same cell after NMDA treatment. RT-PCR revealed that expression of HMGB1 and TNF-alpha was upregulated following SCI. Immunohistochemical examination revealed that the numbers of HMGB1-, TNF-alpha-, and Rage-positive cells were increased following SCI. The number of TUNEL-positive cells was significantly increased at 12 hours after injury, and was maximal at 72 hours after injury. However, HMGB1- and TNF-alpha-positive cells were maximal in number 48 hours after injury, while Rage-positive cells were maximal in number at 24 hours after injury. These data suggest that HMGB1, TNF-alpha, and Rage were upregulated following SCI but preceding the apoptotic cell death. CONCLUSION: Our findings suggest that HMGB1 play a role in the induction of apoptosis via inflammatory reaction.

Stress deprivation from the patellar tendon induces apoptosis of fibroblasts in vivo with activation of mitogen-activated protein kinases.

The effect of stress deprivation on the tendon tissue has been an important focus in the field of biomechanics. However, less is known about the in vivo effect of stress deprivation on fibroblast apoptosis as of yet. This study was conducted to test a hypothesis that complete stress deprivation of the patellar tendon induces fibroblast apoptosis in vivo with activation of Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38) within 24 h after treatment. A total of 35 mature rabbits were divided into stress-shielded (n=15), sham-operated (n=15), and control (n=5) groups. To completely shield the patellar tendon from stress, we used an established surgical method. Animals were sacrificed at 24 h, and 2, 4, 7, and 14 days after the treatment. Tendon specimens underwent TUNEL assay and immunohistological examinations of active caspase-3, JNK, and p38. Both the number and the ratio of TUNEL-positive and caspase-3-positive cells were significantly greater (p<0.0001) in the stress-shielded group than in the sham group at 24 h, 2, 4, and 7 days. Concerning JNK and p38, both the number and the ratio were significantly greater (p<0.0001) in the stress-shielded group than in the sham group at 24 h, 2, and 4 days. This study demonstrated that complete stress deprivation induces fibroblast apoptosis in vivo with activation of JNK and p38 within 24 h. This fact suggested that the fibroblast apoptosis caused by stress deprivation is induced via the mitogen-activated protein kinase signaling pathway.