Imaging well-differentiated hepatocellular carcinoma with dynamic triple-phase helical computed tomography.

To investigate the imaging appearance of well-differentiated hepatocellular carcinoma (HCC) on dynamic CT, a total of 38 histopathologically proven well-differentiated HCC were included in a retrospective study. We reviewed the contrast-enhanced dynamic CT of all 38 tumours for attenuation of each tumour in unenhanced scan, arterial-dominant and delayed portal venous phases. Our results showed that dynamic CT identified 26 (68.4%) out of the 38 lesions. The remaining 12 lesions were isodense compared with surrounding liver parenchyma in each dynamic CT phase. There was no statistically significant difference between the mean size of tumours detected by dynamic CT and that of tumours not detected by dynamic CT (p = 0.1). Of a total of 38 tumours, most were isodense (n = 19) or hypodense (n = 16) in unenhanced scan, mostly hyperdense (n = 18) or isodense (n = 15) in arterial-dominant phase and mostly isodense (n = 22) or hypodense (n = 15) in delayed portal venous phase. Enhancement of tumour was observed in 19 (50.0%) of 38 lesions. In conclusion, the ability of dynamic CT to detect well-differentiated HCC is poor, and negative CT findings cannot exclude the presence of well-differentiated HCC, especially if there is well-grounded clinical suspicion for HCC.

Depiction of vasculature in small hepatocellular carcinoma, and dysplastic nodules evaluated with carbon dioxide ultrasonography and angiography.

PURPOSE: To evaluate the vascularity in dysplastic nodules and well-differentiated and moderately to poorly differentiated hepatocellular carcinomas (HCCs) less than 2 cm using carbon-dioxide (CO2) US and angiography. MATERIAL AND METHODS: A total of 115 pathologically proven small liver tumors (0.7 approximately 2.0 cm) were included in the study. There were 31 dysplastic nodules, 49 well-differentiated HCCs and 35 moderately to poorly differentiated HCCs. A comparative study of angiography and CO2 US was carried out. RESULTS: Of the dysplastic nodules, 28 out of 31 tumors were hypo- or isovascular at CO2 US. Twenty-seven out of 31 tumors were hypovascular at angiography. Of the well-differentiated HCCs, 38/49 showed hypervascularity at CO2 US while 24/49 tumors were hypervascular at angiography. All moderately to poorly differentiated HCCs showed hypervascularity at CO2 US, compared to 30/35 tumors at angiography. CONCLUSION: Most of the dysplastic nodules were hypovascular and most of the moderately to poorly differentiated HCCs were hypervascular. The vascularity of well-differentiated HCCs was in between the above tumors. Both CO2 US and angiography were equally effective in demonstrating the vascularities in dysplastic nodules and moderately to poorly differentiated HCCs. CO2 US was significantly superior to angiography when identifying the vascularity in well-differentiated HCCs.

Paget's disease of the bone: a case report.

Paget's disease of bone is rare in Asia. We report a case of Paget's disease in a 58-year-old Taiwanese man who was admitted with a 3-month history of bilateral numbness in the buttock region. Laboratory data disclosed an elevated serum alkaline phosphatase level (510 U/L). Plain radiographs of the lumbar spine showed generalized increased density at the third lumbar vertebra, associated with cortical thickening, loss of cortico-cancellous definition, and increased anteroposterior diameter. The T1-weighted magnetic resonance image of the lumbar spine showed diffuse, heterogeneous low signal intensity at the third lumbar vertebral body, pedicle, laminae, and spinal process; these areas showed mixed high and low signal intensity on the T2-weighted image. Technetium-99m bone scan revealed abnormal uptake in the involved vertebra. Histologic examination of the third lumbar spinal process confirmed the diagnosis of Paget's disease of bone. The patient remained well during a follow-up period of 6 months.

Quantitative analysis of CDKN2, p53 and retinoblastoma mRNA in human gastric carcinoma.

The mRNA level of CDKN2 (p16), retinoblastoma (Rb) and p53 in cancerous and non-cancerous tissue samples were compared using a semi-quantitative reverse-transcription-polymerase chain reaction method. The mean CDKN2 mRNA level of 10 gastric cancer specimens was significantly higher than that of their non-cancerous tissue samples (p=0.039). In contrast, the mRNA levels of Rb and p53 in gastric cancer tissues were both significantly lower than those in their non-cancerous tissue samples. Furthermore, both mRNA ratios of Rb/CDKN2 and p53/CDKN2 were significantly decreased in gastric cancer tissues. Therefore, suppression of both Rb and p53 and overexpression of CDKN2 may be associated with the tumorigenesis of gastric cancer.

Characterization of glycine-N-methyltransferase-gene expression in human hepatocellular carcinoma.

Messenger RNA differential display was used to study liver-gene expression in paired tumor and non-tumor tissues from hepatocellular carcinoma (HCC) patients. mRNA differential display and Northern-blot analyses showed that a 0.8-kb cDNA fragment was diminished or absent from the tumorous tissues of 7 HCC patients. The cDNA fragment was sequenced and found to have 98.7% nucleotide sequence homology with human glycine-N-methyltransferase cDNA (GNMT). In addition, there was no detectable level of GNMT expression in 4 human HCC cell lines, SK-Hep1, Hep 3B, HuH-7 and HA22T, examined by Northern-blot assay. A full-length GNMT cDNA clone-9-1-2 was obtained by screening a Taiwanese liver cDNA library. In comparison with the GNMT cDNA sequence reported elsewhere, clone 9-1-2 had 4 nucleotide differences resulting in 1 amino-acid change. Immunohistochemical staining with rabbit anti-recombinant GNMT serum showed that GNMT protein almost completely disappeared in liver-cancer cells, while it was abundant in the non-tumorous liver cells. Down-regulation of GNMT gene expression may be involved in the pathogenesis of liver cancer.

Frequent detection of aberrant RNA transcripts of the CDKN2 gene in human gastric adenocarcinoma.

The tumor-suppressor gene CDKN2 (p16/INK4A/MTS1) is frequently altered in human gastric-cancer cell lines. However, mutation of the CDKN2 gene in primary human gastric-carcinoma tissues as seen through genomic DNA analysis has rarely been reported. In this study, a method combining reverse transcription and nested polymerase chain reaction was developed to detect different RNA transcripts of the CDKN2 gene in human gastric cancers. The results showed that, besides the wild-type CDKN2 transcript, 5 of 11 (45.5%) diffuse-type and 3 of 10 (30%) intestinal-type primary gastric adenocarcinoma had aberrant CDKN2 RNA transcripts. Among these 8 tumorous specimens with abnormal CDKN2 RNA transcripts, 6 had intragenic deletions of part of both CDKN2 exons 1 and 2, including 1 case which had an additional inserted sequence from part of CDKN2 intron 2. In addition, 1 case had a deletion of part of CDKN2 exon 1 and 1 case had its entire exon 2 deleted. In contrast, matched normal gastric mucosal tissues from the same patients did not have any aberrant CDKN2 RNA transcript. Furthermore, CDKN2 exon 1 or 2 genomic DNA from all the gastric-carcinoma tissues were PCR-amplified and sequenced and no genetic alteration was detected. Therefore, alteration and heterozygous expression of CDKN2 appears to be involved in the pathogenesis of human gastric cancers.

Clinical experience of esophageal ulcers and esophagitis in AIDS patients.

In Taiwan, numbers of patients with the acquired immunodeficiency syndrome (AIDS) have been increasing in recent years. We present esophageal disease of different causes in 5(16%) heterosexual men among 31 AIDS patients over a 5-year period. Major symptoms included mild dysphagia in 4 (80%) patients and odynophagia in 3 (60%) patients. The duration of symptoms varied from 3 days to 6 months. The symptoms occurred before the diagnosis of AIDS in 3 patients. At esophagogastroduodenoscopy (endoscopy), all 5 patients had esophagitis and/or esophageal ulcers proved by histopathologic evaluation. Four had Candida esophagitis, 3 had cytomegalovirus esophagitis/ulcers and 2 had idiopathic esophageal ulcerations (IEU). Three patients had different esophagitis/ulcers at the same time or during follow-up. The median CD4 lymphocyte count at the time of diagnosis of esophageal disease was 12.2 cells/mm3 (range, 3 to 35 cells/mm3). The endoscopic pictures of the different causes of esophagitis/ ulcers lack uniformity in number, size and appearance. These observations make a conclusion that all AIDS patients with an esophageal disease should undergo endoscopy with biopsy to obtain a definitive diagnosis.

Disseminated Penicillium marneffei infection in a patient with acquired immunodeficiency syndrome.

Penicillium marneffei is a rare human pathogen in Southeast Asia and Southern China. A 26-year-old heterosexual male had intermittent fever, diarrhea and weight loss for 3 months. He was severely immune deficient (CD4+ count, 4/microL) and serologic tests for antibodies against human immunodeficiency virus type-1 were positive. P. marneffei infection was disseminated with involvement of the liver, spleen and bone marrow. The diagnosis was established by histologic examination and confirmed by isolation of the fungus. This infection responded well to amphotericin B. He was discharged with maintenance therapy of itraconazole and continued to be stable during his 2-month follow-up.

Congestive gastropathy in cirrhotic patients: correlation between endoscopic and histological findings.

Congestive gastropathy is a common cause of gastrointestinal bleeding in cirrhotic patients. Forty-six patients with cirrhosis of the liver and 225 control subjects matched in age and sex without cirrhosis of the liver entered the study. We studied the prevalence of congestive gastropathy in cirrhotic patients, and the relationship between endoscopic and histological findings. Congestive gastropathy seen endoscopically was found to be more common in the cirrhotic group than in the control (85% vs. 5%, P < 0.05). The sensitivity, specificity and positive predictive value were 85%, 95% and 76%, respectively. The presence of endoscopic congestive gastropathy was correlated with the severity of liver disease (P < 0.05), but not to the etiology of cirrhosis and the size of esophageal varices with or without red color sign. Endoscopic congestive gastropathy showed no correlation with the histological features including gastritis, interstitial edema, vessel ectasia/congestion and hemosiderin in endoscopic biopsy specimens. In conclusion, congestive gastropathy is a common finding in cirrhotic patients. Its appearance is closely correlated with the severity of liver disease. There is no good correlation between endoscopic congestive gastropathy and mucosal histology.

The rat c-kit ligand, stem cell factor, induces the development of connective tissue-type and mucosal mast cells in vivo. Analysis by anatomical distribution, histochemistry, and protease phenotype.

Mast cell development is a complex process that results in the appearance of phenotypically distinct populations of mast cells in different anatomical sites. Mice homozygous for mutations at the W or S1 locus exhibit several phenotypic abnormalities, including a virtual absence of mast cells in all organs and tissues. Recent work indicates that W encodes the c-kit tyrosine kinase receptor, whereas S1 encodes a c-kit ligand that we have designated stem cell factor (SCF). Recombinant or purified natural forms of the c-kit ligand induce proliferation of certain mast cell populations in vitro, and injection of recombinant SCF permits mast cells to develop in mast cell-deficient WCB6F1-S1/S1d mice. However, the effects of SCF on mast cell proliferation, maturation, and phenotype in normal mice in vivo were not investigated. We now report that local administration of SCF in vivo promotes the development of connective tissue-type mast cells (CTMC) in the skin of mice and that systemic administration of SCF induces the development of both CTMC and mucosal mast cells (MMC) in rats. Rats treated with SCF also develop significantly increased tissue levels of specific rat mast cell proteases (RMCP) characteristic of either CTMC (RMCP I) or MMC (RMCP II). These findings demonstrate that SCF can induce the expansion of both CTMC and MMC populations in vivo and show that SCF can regulate at least one cellular lineage that expresses c-kit, the mast cell, through complex effects on proliferation and maturation.

The Southern California Postrotary Nystagmus Test and electronystagmography under different conditions of visual input.

This study assessed the Southern California Postrotary Nystagmus Test (SCPNT)-stimulated nystagmus under three conditions of indoor illumination (bright, dim, and dark), and it studied the concurrent validity of SCPNT and electronystagmographic (ENG) measures of nystagmus duration and excursion. Eighteen adult subjects received three sets of rotations to the left under different lighting conditions in a counterbalanced order. The duration and excursion of the SCPNT were monitored under the bright and dim conditions, and ENG-recorded duration, excursion, frequency, slow-phase velocity, and average intersaccadic interval were measured under all three lighting conditions. No significant differences were found between nystagmus duration or excursion under the bright and dim conditions, but highly significant differences were found between the dark condition and the other two conditions. The correlation between ENG-recorded duration and SCPNT visually monitored duration across bright and dim conditions was .73, and the correlation for excursion was .24. These results suggest that occupational therapy researchers and clinicians need not question the validity of ENG recordings under different indoor lighting conditions, and suggest that the concurrent validity of ENG recordings and SCPNT measures requires more study.