Multiple symmetric lipomatosis in the Chinese: ultrasound, CT and MR imaging

We report four cases of multiple symmetric lipomatosis in the Chinese population. We believe that multiple symmetric lipomatosis in the Chinese is not uncommon and may be related to the increasing incidence of alcoholism. The ultrasound appearances of these lipomatous masses are presented for the first time. Heterogeneous echogenic masses with fine fibrous strands that insinuate around fascial planes, lymph nodes and vascular tissues are typical findings. Unlike diseases affecting the Western population, multiple symmetric lipomatosis in the Chinese appears to be limited to the head and neck.     

Lifestyle, gender and occupational status as determinants of dental health behavior

A 23-year-old patient suffered from episodic angioedema of the face and neck, accompanied by diarrhea and abdominal pain. Additionally, the patient had bronchial asthma, recurrent nasal polyps and allergic rhinoconjunctivitis. Blood examination revealed leucocytosis with eosinophilia. Histological studies showed eosinophilic infiltrates in the skin and the gastrointestinal mucosa. Allergic food reactions and parasites were ruled out. With systemic corticosteroid treatment, the clinical symptoms and the eosinophilia disappeared. This case shows some parallels to previously described syndromes (eosinophilic gastroenteritis, Samter's syndrome, episodic angioedema with eosinophilia), but to the best of our knowledge this combination of symptoms has not yet been reported.     

A comparison of reagent strips and the refractometer for measurement of urine specific gravity in hospitalized children

OBJECTIVE: To describe a case of Leydig cell tumor of the testis, discuss the criteria for determining its benign or malignant nature and the clinical features according to patient age and the hormone profile. METHODS/RESULTS: Scrotal US evaluation for an associated pathology incidentally detected a hypoechoic, homogeneous mass with preserved borders. Biological testicular tumor markers were determined and the suspicion of a Leydig cell tumor prompted a hormone study. The diagnosis of Leydig cell tumor was confirmed by intraoperative biopsy and radical orchidectomy was performed. CONCLUSION: In the case described, the ultrasound findings prompted the etiological diagnosis given the characteristics of the lesion. The definitive diagnosis was based on the pathological findings. Although classified as benign Leydig cell tumor, radical orchidectomy is advocated.     

Function of the type V transforming growth factor beta receptor in transforming growth factor beta-induced growth inhibition of mink lung epithelial cells

The type V transforming growth factor beta (TGF-beta) is a 400-kDa nonproteoglycan membrane protein that co-expresses with the type I, type II, and type III TGF-beta receptors in most cell types. The type V TGF-beta receptor exhibits a Ser/Thr-specific protein kinase activity with distinct substrate specificity (Liu, Q., Huang, S. S., and Huang, J. (1994) J. Biol. Chem. 269, 9221-9226). In mink lung epithelial cells, the type V TGF-beta receptor was found to form heterocomplexes with the type I TGF-beta receptor by immunoprecipitation with antiserum to the type V TGF-beta receptor after 125I-TGF-beta affinity labeling or Trans35S-label metabolic labeling of the cells. The kinase activity of the type V TGF-beta receptor was stimulated after treatment of mink lung epithelial cells with TGF-beta. TGF-beta stimulation resulted in the growth inhibition of wild-type mink lung epithelial cells and to a lesser extent of the type I and type II TGF-beta receptor-defective mutants, although higher concentrations of TGF-beta were required for the growth inhibition of these mutants. TGF-beta was unable to induce growth inhibition in human colorectal carcinoma cells lacking the type V TGF-beta receptor but expressing the type I and type II TGF-beta receptors. These results suggest that the type V TGF-beta receptor can mediate the TGF-beta-induced growth inhibitory response in the absence of the type I or type II TGF-beta receptor. These results also support the hypothesis that loss of the type V TGF-beta receptor may contribute to the malignancy of certain carcinoma cells.     

Constitutive expression of mature transforming growth factor beta1 in the liver accelerates hepatocarcinogenesis in transgenic mice

Transforming growth factor beta-1 (TGF-beta1) is a potent inhibitor of hepatocyte growth both in vivo and in vitro. In this study, we analyzed the effects of TGF-beta1 on both naturally occurring and diethylnitrosamine-induced hepatocarcinogenesis using single transgenic TGF-beta1 and double transgenic c-myc/TGF-beta1 mice in which the expression of both transgenes was targeted to the liver. Hepatocellular tumors developed spontaneously in 59% (10 of 17) of the TGF-beta1 mice by 16-18 months of age. Coexpression of TGF-beta1 and c-myc transgenes in the liver accelerated hepatic tumor growth in both the presence and absence of carcinogenic treatment. Moreover, diethylnitrosamine-initiated tumors in the c-myc/TGF-beta1 mice showed a high rate of malignant conversion associated with a reduced expression or lack of TGF-beta receptor type II. The results suggest that overexpression of TGF-beta1 may contribute to liver carcinogenesis and that loss of TGF-beta receptor type II transduced inhibitory growth signals and up-regulation of c-myc are critical steps in liver tumor progression.