The lung, abdominal lymph nodes, and bone are the most common sites of extrahepatic metastatic HCC. Most extrahepatic HCC occurs in patients with advanced intrahepatic tumor stage (stage IVA). Incidental extrahepatic lesions at CT in patients with stage I or II intrahepatic HCC are unlikely to represent metastatic HCC.
Abstract. Mature adult parenchymal hepatocytes, typically of restricted capacity to proliferate in culture, can now enter into clonal growth under the influence of hepatocyte growth factor (scatter factor) (HGF/SF), epidermal growth factor (EGF), and transforming growth factor et (TGFo 0 in the presence of a new chemically defined medium (HGM). The expanding populations of hepatocytes lose expression of hepatocyte specific genes (albumin, cytochrome P450 IIB1), acquire expression of markers expressed by bile duct epithelium (cytokeratin 19), produce TGFot and acidic FGF and assume a very simplified morphologic phenotype by electron microscopy. A major change associated with this transition is the decrease in ratio between transcription factors C/EBPo~ and C/EBP[3, as well as the emergence in the proliferating hepatocytes of transcription factors AP1, NFKB. The liver associated transcription factors HNF1, HNF3, and HNF4 are preserved throughout this process. After population expansion and clonal growth, the proliferating hepatocytes can return to mature hepatocyte phenotype in the presence of EHS gel (Matrigel). This includes complete restoration of electron microscopic structure and albumin expression. The hepatocyte cultures however can instead be induced to form acinar/ductular structures akin to bile ductules (in the presence of HGF/SF and type I collagen). These transformations affect the entire population of the hepatocytes and occur even when DNA synthesis is inhibited. Similar acinar/ductular structures are seen in embryonic liver when HGF/SF and its receptor are expressed at high levels. These findings strongly support the hypothesis that mature hepatocytes can function as or be a source of bipotential facultative hepatic stem cells (hepatoblasts). These studies also provide evidence for the growth factor and matrix signals that govern these complex phenotypic transitions of facultative stem cells which are crucial for recovery from acute and chronic liver injury.
Image artifacts are commonly encountered in clinical ultrasonography (US) and may be a source of confusion for the interpreting physician. Some artifacts may be avoidable and arise secondary to improper scanning technique. Other artifacts are generated by the physical limitations of the modality. US artifacts can be understood with a basic appreciation of the physical properties of the ultrasound beam, the propagation of sound in matter, and the assumptions of image processing. US artifacts arise secondary to errors inherent to the ultrasound beam characteristics, the presence of multiple echo paths, velocity errors, and attenuation errors. The beam width, side lobe, reverberation, comet tail, ring-down, mirror image, speed displacement, refraction, attenuation, shadowing, and increased through-transmission artifacts are encountered routinely in clinical practice. Recognition of these artifacts is important because they may be clues to tissue composition and aid in diagnosis. The ability to recognize and remedy potentially correctable US artifacts is important for image quality improvement and optimal patient care.
Human lung lavage proteins were fractionated by centrifuganon and molecular sieving. An antiserum to the post-albumin fraction of the soluble proteins reacted with a 10 KD protein and this protein was isolated by conventional chromatography. The protein, which has a p1 of 4.8, consists of two 5 KD polypeptides and is rich in glutamic acid, leucine, 5crme, and aspartic acid amino acids. The protein does not bind to concanavalin A, pancreatic elastase, leukocyte elastase, or trypsin, and lacks anti-protease activity. It constitutes about 0.15% of the soluble proteins in lung lavage. Antibodies to the 10 KD protein specifically and exclusively stain Clara cells in human, dog, and rat. Staining of granules of Clara
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