Dupuytren disease of the sole]

The authors discuss the essence of Dupuytren disease occurring in the plantar aponeurosis with literary surveys. They briefly outline the essence of the well-known different theories which endeavour to explain the causes of the development of this disease of unknown etiology. In their article, they deal with its clinical manifestation, histological changes and therapeutical possibilities in connection with the 5 cases treated by them.     

Management of lung and bone metastases from thyroid cancers of differentiated structures

During a period of thirty years (1959-1989) 374 patients underwent surgery for differentiated thyroid carcinoma at the 1st Department of Surgery of the University Medical School in Debrecen. Distant metastases were found in the lungs or bones in 36 patients (9.6%). In 20 patients the first clinical sign of the primary disease was the distant metastasis. The aspects of surgical treatment depended on whether the metastases were solitary or multiple, capable or uncapable of radioiodine uptake. Whereas the majority of pulmonary metastases respond well to 131I-treatment the therapy of bone metastases is multidisciplinary. The 5-year survival rate was 47%, the 10-year one 19%.     

The mechanism of cytolytic and cytostatic activity of benfluron

Benfluron at concentrations of 0.26 and 0.52 mumol l-1 inhibited the formation of V79 colonies in a concentration-dependent way. Diminution of the size of colonies of the treated cells was accompanied by a decrease in protein content per cell. At the same time an increase in metabolic activity was observed. Benfluron blocked the V79 cells in S and G2 phases of the cell cycle and at higher concentrations induced cell lysis documented by alterations in cell membrane permeability and morphology. The in vitro membrane effect of benfluron involved a biphasic modulation of the cardiac sarcolemmal (Na+ + K+)-ATPase activity.     

Detection of carriers of Duchenne and Becker muscular dystrophy using the fluorescence in situ hybridization method

Duchenne and Becker muscular dystrophies (DMD/BMD) are X-linked recessive disorders caused by mutations in the dystrophin gene. A large intragenic deletion has been described in about 65% of DMD/BMD patients. Mothers of affected males are DMD/BMD carriers in two thirds of the cases. Routine deletions detection in DMD/BMD males is performed using multiplex polymerase chain reaction (mPCR), RT-PCR with a protein truncation test (PTT) or using Southern blotting. In females the deletions detection is complicated by the presence of a normal gene copy on the second X-chromosome. We are presenting the diagnostic strategy using FISH for the deletions detection in the dystrophin gene of female DMD/BMD carriers. We have used a set of six cosmid probes for the detection of the most frequently deleted areas of the dystrophin gene from the Department of Human Genetics, Leiden University Medical Center. We have examined 14 mothers of DMD/BMD males with a deletion in the dystrophin gene identified using mPCR. Four mothers of affected males have been diagnosed as carriers of a deletion in the dystrophin gene. We have revealed no deletion mutations in the exons examined in a control group of four healthy females. No discrepancy has been found between the FISH analysis results and the results of mPCR. Our results indicate that FISH is an effective and direct method for the identification of DMD/BMD carriers and we suggest this method as a method of a first choice in the identification of DMD/BMD carriers.     

Transient expression of keratin 19 is induced in originally negative interfollicular epidermal cells by adhesion of suspended cells

Keratin 19 and nuclear reactivity to an endogenous lectin, galectin-1, represent a potential marker of epidermal stem cells. We detected expression of keratin 19 and nuclear binding sites for galectin-1 in adult cells migrating from the hair follicle, where cells expressing keratin 19 are located in the bulge region. The results were compared with the expression of both markers in cells adhering from suspension prepared from the interfollicular epidermis without keratin-19-positive cells and with nuclear binding sites for galectin-1. The results were compared with data from basal cell carcinomas. All cells were analyzed concerning size, as it is known that cell diameter influences the clonogenic potential of keratinocytes. The major result of this study is the observation of transient expression of keratin 19 and nuclear galectin-1 binding sites in originally negative interfollicular epidermal cells induced by adhesion. These cells were very small in size, similar to basal cells of the interfollicular epidermis or the bulge region of the hair follicle. The influence of the suspension regimen on beta1-integrin expression, cell diameter and growth was also monitored. A population of cells highly positive for beta1 integrin of the same diameter as keratin-19-positive cells insensitive to induction of terminal differentiation by lack of anchorage was characterized. Cells of the same size were also observed in the keratin-19-positive cells of basal cell carcinomas. In conclusion, the expression of poor levels of differentiation induced by cell adhesion is transient. Also, keratin 19 expression should not be exclusively regarded as a marker of stem cell activity.     

A Bcl-2-dependent molecular timer regulates the lifespan and immunogenicity of dendritic cells

The lifespan of antigen-bearing dendritic cells (DCs) is determined by signals from pathogens and T cells. These signals regulate DC survival by modulating expression of Bcl-2 family proteins. Toll-like receptors and T cell costimulatory molecules both trigger a DC survival pathway that is dependent on Bcl-x(L). However, Toll-like receptors uniquely increase expression of Bim and trigger cell death by a pathway that is blocked by Bcl-2. This pathway serves as a molecular 'timer' that sets the lifespan of DCs and regulates the magnitude of T cell responses in vivo. Thus, signals derived from the innate and acquired immune systems control DC lifespan and immunogenicity by distinct molecular mechanisms.