Expression of Ah receptor (TCDD receptor) during human monocytic differentiation

We have previously found a high expression of human Ah receptor(TCD receptor) mRNA in peripheral blood cells of individuals.In this paper, the expression of this gene in blood cells wasfirst investigated in fractions of nucleated cells, revealingpredominant expression of the Ah receptor gene in the monocytefraction. Then the expression levels of AhR mRNA in varioushematopoietic cell lines were examined together with those ofArnt and P450IA1. AhR was expressed at high levels in monocytoidU937, THP1, and HEL/S cells, and at moderate levels in promyelocyticHL60 cells and erythroblastic HEL cells. However, it was notdetected in lymphoid cells MOLT4 (T cell) and BALL1 (B cell),nor in K562 erythroblasts. Furthermore, a specific inductionof AhR during monocytic differentiation was investigated inHL60 and HEL cells. HL60 cells were induced to differentiatetoward monocytes-macrophages by incubation with phorbol ester,showing a 5- to 20-fold increase of AhR mRNA. The incubationwith transforming growth factor ß1 and 1     

Endoscopic treatment for benign biliary strictures: Can placement of a covered metallic stent be an option in refractory cases?

Background: Recently, endoscopic treatment has been attempted to counter benign biliary strictures. It is expected to be an alternative to surgical operation because of its lower morbidity and its convenience, but the long‐term results have not yet been sufficiently elucidated. Here, we evaluate the short‐ and long‐term results of endoscopic stenting in patients with benign biliary strictures, and also describe a new technique using a covered metallic stent (CMS) in the refractory cases. Methods: The charts of 22 consecutive patients with benign biliary stricture treated endoscopically at our institutions between December 1995 and December 2002 were analyzed retrospectively. Results: Stricture etiology was as follows: postoperative, nine; chronic pancreatitis, seven; primary sclerosing cholangitis (PSC), three; and other, three. The stent initially placed was a 7 Fr in 11 patients and a 10 Fr in 11 patients. Eighteen of 22 patients (82%) were successfully treated by the initial treatment, and stents were removed after a mean duration of 3.1 months (range: 1–14 months). In the remaining four patients, stents were exchanged once to four times after that, and a CMS was placed as the second endoprosthesis in two patients with chronic pancreatitis. These stents, including CMS, were finally removed from these four patients after a mean duration of 14.8 months (range: 8–22 months). Over a median follow‐up period of 26 months (range: 6–78 months), one recurrence has been observed, in which case a CMS was placed in a patient with chronic pancreatitis. The CMS was removed successfully 6 months after the insertion, and no recurrence was observed during the 6‐month follow‐up period. Conclusions: Endoscopic stenting for benign biliary stricture is an alternative to surgery because it shows satisfactory results. Placement of a CMS would also be an option in refractory strictures, such as those due in chronic pancreatitis, if the certainty of removal is proven by cumulative experience with a large number of patients.     

Retrospective endoscopic study of developmental and configurational changes of early colorectal cancer: Eight cases and a review of the literature

Background: A retrospective endoscopic follow‐up study was conducted to elucidate the development of minute or superficial‐type cancers. Methods: The development of eight colorectal cancers that were followed up by endoscopy was evaluated. Results: (i) Cancer with high‐grade atypia frequently developed from lesions diagnosed histologically by biopsy as adenoma; (ii) two polypoid adenomas developed into invasive cancers with non‐polypoid configuration; (iii) a superficial elevated‐type cancer with high‐grade atypia remained a mucosal cancer for more than 1 year; (iv) a superficial depressed (SD)‐type cancer that had a concomitant adenomatous component grew slowly, maintaining the same configuration for more than 2 years. Another SD‐type cancer grew rapidly to an advanced cancer; and (v) a superficial elevated adenoma developed into a IIa + IIc‐type submucosally invasive cancer while maintaining the size of the initial tumor. From the analysis of the literature, 35 lesions were collected, but it was impossible to speculate which specific type of tumor grew rapidly. Conclusions: From the endoscopic observations of the present study and the review of the literature, developments of superficial type cancers were diverse, sessile‐type cancers with marked configurational change, and early cancers developed slowly, although the speed of their growth accelerated according to the downward invasion of the cancer.     

Prognostic factors of peripheral T-cell lymphoma (PTL): statistical analysis on 30 patients

Peripheral T-cell lymphoma (PTL) is a distinctive clinical entity, albeit it comprises several diseases with histologically heterogeneous diagnoses. We studied prognostic factors on 30 patients diagnosed and treated at Shikoku Cancer Center Hospital. Clinical findings and laboratory data were evaluated by statistical analysis to investigate the important factors influencing survival duration. Variables influencing survival were stage, leukemic change, bone marrow infiltration (BMI), anti-human T-lymphocyte virus-type I antibody, white blood cell count, and lactate dehydrogenase (LDH). Multivariate analysis revealed high level of LDH and positive BMI as the important factors for short survival. Histological classifications of the Working Formulation and the T-lymphoma classification by Suchi et al. were also evaluated whether these were related with prognosis. Our data revealed that there was no significant relationship between histological subtype and survival duration. The study of prognostic factors provides valuable aids for us to understand the clinical characteristics of PTL patients with various backgrounds.     

TGF-beta gene expression in mesangial cells]

TGF-beta recently has been shown to inhibit mesangial cell growth and to stimulate mesangial matrix synthesis by mesangial cells. Cultured rat mesangial cells expressed 2.5 kb TGF-beta mRNA, and removal of fetal calf serum (FCS) for two days decreased the TGF-beta mRNA level, which was then stimulated by addition of 17% FCS and TPA, one of the phorbol esters, although it is also reported by others that the mRNA expression was stimulated by PDGF, EGF, or high glucose. Bioassay and immunoblot analysis showed that mesangial cells produce and secrete substantial amounts of TGF-beta but mostly in latent forms. Moreover, addition of anti-TGF-beta neutralizing antibodies augmented mesangial cell growth, indicating that the secreted TGF-beta exerts a growth-inhibitory action on themselves. Thus, TGF-beta may function as an autocrine factor in mesangial cells, and it is suggested that mesangial cells may play an important role in the pathogenesis of glomerulopathy.     

Development of the endolymphatic sac in chick embryos, with reference to the degradation of otoconia.

The endolymphatic sac of chick embryos (from embryonic day 7 to 1-day-old chicks) was studied light- and electron-microscopically. At stage 30-31 (embryonic day 7-7.5), the epithelial cells of the endolymphatic sac were cuboidal to columnar in shape. Microvilli were relatively well developed. The intercellular space was wide. In the endolymphatic space of the endolymphatic sac, varying shapes and sizes of otoconia-like bodies were often observed. Intracytoplasmic phagosomes containing these bodies were rarely found. After stage 37 (embryonic day 11), otoconia-like bodies in the endolymphatic sac decreased in number and size. They were almost the same as the otoconia in the macular organs, ultrastructurally. These findings indicate that the endolymphatic sac of the chick embryos may possess the function of otoconial degradation and removal of calcium from otoconia.     

Quantitative comparison of aromatase induction by dexamethasone in fibroblasts from a patient with familial cortisol resistance and a patient with cortisol hyperreactive syndrome

The ability of dexamethasone to induce aromatase activity was tested in fibroblasts from a patient with familial cortisol resistance, a patient with cortisol hyperreactive syndrome, and five normal subjects. Dexamethasone increased enzyme activity in all cases in a concentration-dependent manner (over a range of 1-1000 nmol/L). In fibroblasts from a patient with familial cortisol resistance, the response curve of dexamethasone-induced aromatase activity was shifted to the right compared to that of normal cells. However, the maximal induction of the enzyme at 1 mumol/L dexamethasone was unchanged in cortisol-resistant fibroblasts. On the other hand, in fibroblasts from the patient with the cortisol hyperreactive syndrome, the half-maximal effect of dexamethasone was similar to that in normal cells, but maximum induction of aromatase activity was 2 times greater than that in normal cells. The glucocorticoid antagonist RU 486 inhibited dexamethasone-induced aromatase activity in these patients' cells and in normal cells in a concentration-dependent manner, indicating that the altered effects of dexamethasone on aromatase induction observed in each cell type were mediated through glucocorticoid receptors.