Expression of epidermal growth factor and fibroblast growth factor in human hepatocellular carcinoma: an immunohistochemical study.

Expression of epidermal growth factor (EGF) and fibroblast growth factor (FGF) was examined in 56 patients with hepatocellular carcinoma (HCC) using an immunohistochemical method. EGF and FGF were expressed on carcinoma cells in 14 (25%) and 23 cases (41%), respectively. In the 23 FGF-positive cases, 11 cases were positive for both acidic and basic FGF, while 18 were positive for acidic FGF, and 16 were positive for basic FGF. In non-cancerous hepatic tissues, FGF was weakly positive in macrophages, hepatocytes and vascular endothelial cells in some cases, while EGF was totally negative. There were no significant correlations between the expression of EGF or FGF on carcinoma cells and the various clinicopathologic factors examined. These data suggest that EGF and FGF are produced by human HCC cells in vivo. The roles of the expression of these growth factors in the development and progression of HCC remain only speculative.     

Strain Difference of Susceptibility to 4-Nitroquinoline 1-Oxide-induced Tongue Carcinoma in Rats

Strain difference of susceptibility to 4-nitroquinoline 1-oxide (4NQO)-induced squamous cell carcinomas of the tongue among Dark-Agouti, Long-Evans, Sprague-Dawley, ACI/Ms, Fischer 344, Donryu and Wistar/Furth rats was surveyed by evaluating the survival times, incidences and sizes of developed tumors as markers of susceptibility. Administration of 4NQO dissolved in drinking water induced squamous cell carcinomas in various sites of the upper digestive tract mucosa of all the experimental male and female rats of the seven strains. Regarding the mean survival times, Wistar/Furth rats survived much longer than any other strain of rats, and Dark-Agouti showed the shortest survival. The incidence of large, mass-type carcinomas of the tongue of Dark-Agouti rats was higher than in any other strain of rats, while that of Wistar/Furth rats was the lowest. Subsequently the mitotic activity and bromodeoxyuridine incorporation in the tongue epithelium of Dark-Agouti and Wistar/Furth rats were estimated after a short-term administration of 4NQO. There was a pronounced difference between the two strains of rats, because the proliferative responses of the tongue epithelium of Dark-Agouti rats to the 4NQO stimulation were much higher than those of Wistar/Furth rats. These results indicated that there are marked differences in the susceptibility to 4NQO-induced tongue carcinoma among the seven strains of rats, and that Dark-Agouti and Wistar/Furth rats could be useful as models of highly and poorly susceptible strains, respectively, for further genetic analysis.     

Chymase participates in chronic dermatitis by inducing eosinophil infiltration

An epicutaneous application of 2,4-dinitrofluorobenzene (DNFB) to a mouse ear caused a transient skin swelling, and the repetition of the challenge enlarged the contact dermatitis. The repeated challenge with DNFB also induced eosinophil infiltration on the application site. Administration of a chymase inhibitor significantly inhibited the ear swelling as well as eosinophil accumulation. An intradermal injection of human chymase to the mouse ear also elicited transient skin swelling and eosinophil infiltration, both of which were augmented in proportion to the number of injections. Human serum albumin and heat-inactivated chymase failed to induce such skin reactions, suggesting the participation of proteolytic activity of the enzyme. In addition, chymase stimulated eosinophil migration in vitro in a concentration-dependent manner. Taken together, these observations suggest that mast cell chymase may contribute to development of the DNFB-induced dermatitis, probably by promoting eosinophil infiltration. It is therefore possible that chymase plays a role in pathogenesis of chronic dermatitis such as atopic dermatitis.     

An Epstein-Barr virus-producer line Akata: Establishment of the cell line and analysis of viral DNA

An Epstein-Barr virus (EBV)-producer line, designated Akata, was established from a Japanese patient with Burkitt's lymphoma. The Akata line possessed the Burkitt's-type chromosome translocation, t(8q-; 14q+), and was derived from the tumor cell. Akata cells produced a large quantity of transforming virus upon treatment of cells with anti-immunoglobulin antibodies (Takada, 1984). Southern blot analysis of viral DNA indicated that the Akata EBV is nondefective and more representative of wild-type viruses. Akata cells should be useful as a source of EBV.     

中药对大鼠自发性慢性胰腺炎的干预作用及其方证病态基础

目的探讨桂枝汤、柴胡桂枝汤、小柴胡汤和卡莫司他对大鼠自发性慢性胰腺炎的干预作用及其方证病态基础。方法57只雄性4周龄WBN/Kob大鼠随机分为5组模型组、桂枝汤组、柴胡桂枝汤组、小柴胡汤组和卡莫司他组,每组大鼠均予以相应药物干预,共12周。每4周取大鼠胰腺组织观察胰腺湿重;HE染色观察胰腺组织病理学改变;RT-PCR技术检测大鼠胰腺胰腺炎相关蛋白(pancreatitis-associatedprotein,PAP)mRNA的表达水平;免疫组织化学方法检测胰腺PAP蛋白的表达。结果模型组自12周龄起胰腺组织发生胰腺炎病理学改变;桂枝汤组未观察到胰腺炎病理学改变;小柴胡汤组和卡莫司他组在16周龄时,胰腺组织均发生明显的胰腺炎病理学改变。桂枝汤组抑制PAPmRNA表达的作用大于其他各中药干预组。桂枝汤组和柴胡桂枝汤组在12周龄时,未发现胰腺PAP的表达。结论桂枝汤、柴胡桂枝汤、小柴胡汤和卡莫司他对大鼠自发性慢性胰腺炎具有不同程度的防治作用,其中以桂枝汤的作用最为明显。“太阳表证”可能是大鼠自发性慢性胰腺炎的中医基本证候病机,PAP的表达可能是其证候病机的病态基础之一。     

Immunolocalisation of PIVKA-II in paraffin-embedded specimens of hepatocellular carcinoma

Abstract: Aims/Background: Although serum PIVKA-II has been widely used as a tumor marker for hepatocellular carcinoma (HCC), little information is available concerning tissue PIVKA-II, and detection of tissue PIVKA-II in paraffin-embedded tissue specimens of HCC is also considered difficult. Methods: Paraffin-embedded HCC tissues obtained at autopsy from 22 patients were subjected to immunohistochemical staining using the antibody MU-3 (Eisai Co., Ltd.) after microwave antigen retrieval. Results: PIVKA-II was mainly detected in the cytoplasm of HCC cells. The intensity of tissue PIVKA-II staining was not correlated with serum PIVKA-II levels or with the histological differentiation of HCC. However PIVKA-II staining tended to be more intense in tissue from patients with portal tumor thrombus, distant metastases, or a longer duration of HCC. Conclusion: This method of immunohistochemical staining is easy and simple to use and may be helpful for detecting tissue PIVKA-II in paraffin-embedded HCC specimens.     

EUS and K-ras analysis of pure pancreatic juice collected via a duodenoscope after secretin stimulation for diagnosis of pancreatic mass lesion: a prospective study

BACKGROUND: The early diagnosis of pancreatic cancer remains problematic. This prospective study assessed the utility of a combination of endoscopic ultrasound (EUS) and genetic analysis of pure pancreatic juice in the diagnosis of pancreatic mass lesions. METHODS: One hundred seventy-six patients with suspected pancreatic disease were enrolled and underwent ultrasonography (US), computed tomography (CT), endoscopic retrograde choleangiopancreatography (ERCP), and EUS. Pure pancreatic juice was collected endoscopically after secretin stimulation. K-ras point mutations at codon 12 in the juice were assayed by polymerase chain reaction-restriction fragment length polymorphism. RESULTS: Thirty-six (20%) patients were found to have solid pancreatic masses including 19 with cancer (7 patients, 相似文献   

P8 expression is induced in acinar cells during chronic pancreatitis

The p8 gene is barely expressed in the normal pancreas, but is overexpressed in acute pancreatitis. To elucidate the dynamic expression of p8 mRNA and its significance in the course of chronic pancreatitis, we investigated the p8 expression in spontaneous chronic pancreatitis in the WBN/Kob rat as well as in humans and arginine-treated rat pancreatic acinar AR4-2J cells. p8 mRNA was significantly increased at 12 weeks when chronic pancreatitis first appeared in the WBN/Kob rats. p8 was immunolocalized in the acinar cell nuclei. Acinar cell apoptosis was significantly increased at 12 and 20 weeks in the WBN/Kob rats. In AR4-2J cells, p8 mRNA was significantly induced at 4 hr after arginine addition. Apoptosis of AR4-2J cells was not increased during the strong expression of p8 mRNA. These results suggest that p8 is induced in the acinar cells during chronic pancreatitis as the self-defence mechanism against proapoptotic insults.