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R Fawaz

Publications and source records attributed to R Fawaz.

8 recordsLinked to original sources
PubMed2000

Cytokeratin 7 and 20 expression in cholangiocarcinomas varies along the biliary tract but still differs from that in colorectal carcinoma metastasis.

In the liver, the immunostaining of cytokeratins (CK) 7 and 20 has been used to distinguish usual peripheral cholangiocarcinomas (CC) and colorectal carcinoma metastasis (CRM). However, other subtypes of CC are not infrequent and may be particularly difficult to distinguish from CRM by histology and even immunohistochemistry. Therefore, 48 CC from different locations, either peripheral (n = 19), or nonperipheral, that is, from the large intrahepatic bile ducts, the hilum, and the extrahepatic bile ducts (n = 29), and with different cytoarchitectural patterns were tested for CK7 and CK20 and compared with 31 CRM. CC were positive for CK7 and CK20 in 96% and 70%, respectively, whatever the architecture and differentiation of the tumor. The labeling index (LI) of CK7 in CC was always high, whereas it was low or moderate for CK20. CK20-positive phenotype was significantly more frequent in nonperipheral than in peripheral CC (82% vs 47%; p = 0.007). CRM were all positive for CK20 with a high LI, and mostly negative (81%) for CK7. In conclusion, (1) the CK immunoprofile of CC varies according to the location of the tumor in the biliary tract, peripheral CC being more often CK7+/CK20-, and nonperipheral ones CK7+/CK20+; and (2) a decision tree based on CK20 LI and CK7 positivity allows the distinction of CRM and CC, even for the nonperipheral type.

Adult↗
PubMed1999

Real-time control of focused ultrasound heating based on rapid MR thermometry.

RATIONALE AND OBJECTIVES: Real-time control of the heating procedure is essential for hyperthermia applications of focused ultrasound (FUS). The objective of this study is to demonstrate the feasibility of MRI-controlled FUS. METHODS: An automatic control system was developed using a dedicated interface between the MR system control computer and the FUS wave generator. Two algorithms were used to regulate FUS power to maintain the focal point temperature at a desired level. RESULTS: Automatic control of FUS power level was demonstrated ex vivo at three target temperature levels (increase of 5 degrees C, 10 degrees C, and 30 degrees C above room temperature) during 30-minute hyperthermic periods. Preliminary in vivo results on rat leg muscle confirm that necrosis estimate, calculated on-line during FUS sonication, allows prediction of tissue damage. CONCLUSIONS. The feasibility of fully automatic FUS control based on MRI thermometry has been demonstrated.

Animals↗
PubMed1996

Morphology of hepatic stellate cells in patients with fulminant or subfulminant hepatitis requiring liver transplantation.

Hepatic stellate cells were studied by immuno-cytochemistry with anti smooth muscle alpha-actin antibody (an activation marker for these cells) and electron microscopy, in eleven patients transplanted for fulminant or subfulminant hepatitis. Numerous smooth muscle alpha-actin positive cells were found in necrotic areas. In both fulminant and subfulminant hepatitis, hepatic stellate cells appeared enlarged, often irregular, with spikes. There were numerous signs of activation and many contained numerous small lipid droplets. In the cases of fulminant hepatitis, hepatic stellate cells presented, at times, some subcellular damage. Hepatic stellate cells processes, often in several layers, displayed numerous cytoplasmic microfilaments with conspicuous dense plaques below the plasma membrane. Hepatic stellate cells were never surrounded by a basement membrane. The extracellular matrix was loose and granulofibrillar. In areas of multiacinar nodules (in cases of map-like pattern), hepatic stellate cells were grossly normal. These results are in agreement with in vitro data showing that acutely damaged hepatocytes activate hepatic stellate cells but do not fully transform them into myofibroblasts.

Acetaminophen↗
PubMed1994

Preservation of human liver grafts in UW solution. Ultrastructural evidence for endothelial and Kupffer cell activation during cold ischemia and after ischemia-reperfusion.

Biopsies taken from 13 human liver grafts at different stages of the transplantation process were used for study of the morphology of sinusoidal cells prior to harvesting (5 biopsies), after preservation in UW solution (10 biopsies), and after complete revascularization (13 biopsies). The mean cold ischemic period was 12 h 30. Immediate follow up was uneventful and the mean peak of post-operative transaminases below 1300 IU/l. Biopsies were perfusion-fixed by the transparenchymal route to ensure satisfactory ultrastructural results. There were no loose sinusoidal endothelial cells in the lumen and no signs of cellular death. Some endothelial cells presented signs of activation at the end of the preservation period, and even more after revascularization, with numerous lucent vacuoles resembling endosomes in the cytoplasm. Kupffer cells also presented signs of activation, particularly after reperfusion. The retraction of endothelial cell processes which formed large gaps during cold ischemia proved to be partly reversible after reperfusion. Signs of endothelial cell damage with gaps and partial rupture of the plasmic membrane were also observed, particularly after revascularization, in areas which contained numerous inflammatory cells adhering to the wall. The Disse space was not generally enlarged and contained no inflammatory cells. The sinusoidal pole of hepatocytes was occasionally damaged with the formation of blebs. These results strongly suggest that any drug or preservation solution that will inhibit endothelial and Kupffer cell activation could be beneficial in the prevention of preservation and reperfusion injury.

Adenosine↗
PubMed1994

Ultrastructure of human liver grafts preserved with UW solution. Comparison between patients with low and high postoperative transaminases levels.

We studied the morphology of sinusoidal cells on 21 human liver grafts prior to harvesting, at the end of the preservation period in UW solution, and after complete revascularization. The mean cold ischemic period was 11 h 34 min. Immediate follow-up was uneventful in 20 of these cases; 13 showed a mean peak of postoperative transaminases below 1,300 IU/L (group A), and 7 above 1,500 IU/L (group B). In the case of one patient (group C) steatosis was severe (50%) and there was serious postoperative dysfunction (transaminases 18,000 IU/L). Biopsies were perfusion-fixed by the transparenchymal route to ensure satisfactory ultrastructural results. In group A, some sinusoidal endothelial cells presented signs of activation at the end of the preservation period, and even more after revascularization. Kupffer cells also presented signs of activation particularly after reperfusion. Signs of endothelial cell damage with gaps and partial rupture of the plasmic membrane were also observed, particularly after revascularization in areas which contained numerous inflammatory cells adhering to the wall. The sinusoidal pole of hepatocytes was occasionally damaged, with the formation of blebs. In group B, adhesion of inflammatory cells to the sinusoidal wall was increased. Furthermore, in some areas with endothelial cell damage, neutrophils and platelets infiltrated the Disse space, and hepatocytes were increasingly damaged. In the case of patient C, the most obvious signs after reperfusion were hepatocyte drop out and death but there was no evidence of any concomitant sinusoidal cell damage. It would appear that even in cases where immediate follow-up is eventful, endothelial and Kupffer cells show signs of activation. This can be associated with signs of microcirculatory disturbances as was seen in 4 cases in group B. In the only case of severe steatosis that we studied, the essential sign was death of hepatocytes.

Adenosine↗