Evaluation of Temperature Distribution Around the Probe in Cryoablation of Lipiodol-Mixed-Tissue Phantom.

PURPOSE: To determine whether lipiodol, which has low thermal conductivity, influences ice ball formation during cryoablation of a lipiodol-mixed-tissue phantom. MATERIALS AND METHODS: Lipiodol-mixed-tissue phantoms were created by injecting lipiodol (4-6 ml) into the renal arteries of ex vivo porcine kidneys (lipiodol group). A cryoprobe (CryoHit™ Needle S) with a holder that was set with thermocouples at various positions around the cryoprobe was inserted. After freezing for 300 s, the followings were evaluated: ice ball size on CT, temperature distribution around the cryoprobe, and calculated distances at 0 °C and - 20 °C. Each variable was compared between lipiodol group (n = 6) those obtained in a control group without lipiodol injection (n = 6). RESULTS: Mean ice ball diameter (width/length) on CT was 22.1 ± 2.3/22.9 ± 2.3 mm in the lipiodol group and 21.6 ± 0.7/22.2 ± 1.3 mm in the control group. Mean cryoprobe temperature was - 118 ± 3.0 °C in the lipiodol group and - 117 ± 2.6 °C in the control group. In both groups, temperature at the 3 mm thermocouple reached approximately - 50 °C and was < 0 °C within ~ 10 mm of the cryoprobe. Temperature of 0/- 20 °C occurred at a mean distance from the cryoprobe of 11.1 ± 0.5/6.9 ± 0.4 mm in the lipiodol group and 11.0 ± 0.2/6.9 ± 0.2 mm in the control group. There was no significant difference in any variable between the groups. CONCLUSION: The inclusion of lipiodol in a tissue phantom had no negative effects on ice ball formation that were related to thermal conductivity.

Fundamental Evaluation of Thermophysical Properties of Lipiodol Associated with Cryoablation: Freezing Experiments Using Lipiodol Phantom.

PURPOSE: To elucidate the basic thermophysical properties at low temperatures of lipiodol, which is used as a marker by transarterial injection before CT-guided cryoablation for solid tumors, by fundamental experiments with pure lipiodol phantom. MATERIALS AND METHODS: The freezing point of lipiodol was measured using differential scanning calorimeter (DSC) by detecting differences in the heating rate during heating from - 30 °C. Freezing experiments were conducted using pure lipiodol and a tissue phantom, which were prepared in an acrylic container at 37 °C. The growth of the frozen region was observed for 10 min. Temperatures were monitored at the cryoprobe surface and designated positions around the cryoprobe. RESULTS: The DSC experiment showed that freezing was observed between - 5 and - 30 °C, which indicated that the freezing point was approximately - 5 °C. Freezing experiments revealed that the diameter of frozen region in the lipiodol was smaller than that in the tissue phantom (5 mm vs 24 mm) after 10-min freezing. The temperature at the probe surface was - 130 °C in lipiodol, which was 25 °C lower than that in the tissue phantom. There was a larger temperature gradient near the cryoprobe in lipiodol due to lower thermal conductivity. CONCLUSIONS: The present results suggest that an extremely high concentration of lipiodol (close to pure lipiodol) potentially reduces frozen region because of its lower freezing point and smaller thermal conductivity. However, since lipiodol concentrations in clinical cases differ from the current model, further studies using models that are close to clinical conditions are required. LEVEL OF EVIDENCE: No level of evidence, laboratory investigation.

In-situ measurement of the heat transport in defect- engineered free-standing single-layer graphene.

Utilizing nanomachining technologies, it is possible to manipulate the heat transport in graphene by introducing different defects. However, due to the difficulty in suspending large-area single-layer graphene (SLG) and limited temperature sensitivity of the present probing methods, the correlation between the defects and thermal conductivity of SLG is still unclear. In this work, we developed a new method for fabricating micro-sized suspended SLG. Subsequently, a focused ion beam (FIB) was used to create nanohole defects in SLG and tune the heat transport. The thermal conductivity of the same SLG before and after FIB radiation was measured using a novel T-type sensor method on site in a dual-beam system. The nanohole defects decreased the thermal conductivity by about 42%. It was found that the smaller width and edge scrolling also had significant restriction on the thermal conductivity of SLG. Based on the calculation results through a lattice dynamics theory, the increase of edge roughness and stronger scattering on long-wavelength acoustic phonons are the main reasons for the reduction in thermal conductivity. This work provides reliable data for understanding the heat transport in a defective SLG membrane, which could help on the future design of graphene-based electrothermal devices.

Effect of irreversible electroporation on three-dimensional cell culture model.

Irreversible electroporation (IRE) is a new treatment to necrotize abnormal cells by high electric pulses. Electric potential difference over 1 V across the plasma membrane permanently permeabilizes the cell with keeping the extracellular matrix intact if the thermal damage due to the Joule heating effect is avoided. This is the largest advantage of the IRE compared to the other conventional treatment. However, since the IRE has just started to be used in clinical tests, it is important to predict the necrotized region that depends on pulse parameters and electrode arrangement. We therefore examined the numerical solution to the Laplace equation for the static electric field to predict the IRE-induced cell necrosis. Three-dimensionally (3-D) cultured cells in a tissue phantom were experimentally subjected to the electric pulses through a pair of puncture electrodes. The necrotized area was determined as a function of the pulse repetition and compared with the area that was estimated by the numerical analysis.

Evidence for osteocyte regulation of bone homeostasis through RANKL expression.

Osteocytes embedded in bone have been postulated to orchestrate bone homeostasis by regulating both bone-forming osteoblasts and bone-resorbing osteoclasts. We find here that purified osteocytes express a much higher amount of receptor activator of nuclear factor-κB ligand (RANKL) and have a greater capacity to support osteoclastogenesis in vitro than osteoblasts and bone marrow stromal cells. Furthermore, the severe osteopetrotic phenotype that we observe in mice lacking RANKL specifically in osteocytes indicates that osteocytes are the major source of RANKL in bone remodeling in vivo.

Blimp1-mediated repression of negative regulators is required for osteoclast differentiation.

Regulation of irreversible cell lineage commitment depends on a delicate balance between positive and negative regulators, which comprise a sophisticated network of transcription factors. Receptor activator of NF-kappaB ligand (RANKL) stimulates the differentiation of bone-resorbing osteoclasts through the induction of nuclear factor of activated T cells c1 (NFATc1), the essential transcription factor for osteoclastogenesis. Osteoclast-specific robust induction of NFATc1 is achieved through an autoamplification mechanism, in which NFATc1 is constantly activated by calcium signaling while the negative regulators of NFATc1 are suppressed. However, it has been unclear how such negative regulators are repressed during osteoclastogenesis. Here we show that B lymphocyte-induced maturation protein-1 (Blimp1; encoded by Prdm1), which is induced by RANKL through NFATc1 during osteoclastogenesis, functions as a transcriptional repressor of anti-osteoclastogenic genes such as Irf8 and Mafb. Overexpression of Blimp1 leads to an increase in osteoclast formation, and Prdm1-deficient osteoclast precursor cells do not undergo osteoclast differentiation efficiently. The importance of Blimp1 in bone homeostasis is underscored by the observation that mice with an osteoclast-specific deficiency in the Prdm1 gene exhibit a high bone mass phenotype caused by a decreased number of osteoclasts. Thus, NFATc1 choreographs the determination of cell fate in the osteoclast lineage by inducing the repression of negative regulators as well as through its effect on positive regulators.