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C de Greef

Publications and source records attributed to C de Greef.

9 recordsLinked to original sources

[Report of 243 vertical mammoplasties for very large, heavy breasts and/or severe ptosis. Analysis of the result and technical].

Vertical mammaplasties for very large breasts and/or severe ptosis were evaluated in 124 patients who underwent operation in our unit between September 1993 and June 2001. In 119 cases it was reduction mammaplasty and in 5 cases unilateral symmetrization after contralateral reconstruction. The mean age was 36 years (13-62 years). Among inclusion criteriae, we choose the resection weight > or = 700 g and/or a ptosis > or = 30 cm. We report a few technical modifications of the initial Lejour vertical technique. About hypertrophic breasts (179 breasts): mean resection weight was 905 g (710-1750 g), mean ptosis was 33.5 cm (30-42 cm). The following complications were noted: 3 haematomas with only one evacuation on the same day, no seroma, 4 infections controlled by local treatment, 44 wound dehiscence or delayed skin healing (> 30 d), 8 partial necrosis, 12 secondary correction under local anaesthesia, 1 cheloïd scar of the areolar complex. About breasts with severe ptosis (64 breasts): the mean value was 31.8 cm (30 cm). Complications were as follow: 2 haematoma, 0 seroma, 16 healing delay, 3 partial necrosis, 6 secondary correction under local anaesthesia. The mean procedure time was 94 mn. The mean stay in hospital was 2.8 days, same as the suction drains. The vertical mammaplasty is a fast technique, giving good results. Scarring amount is reduced. Breasts are well projected, well shaped and remain stable in time. Their base can be modified. We think this technique can safely be applied to large breasts and/or severe ptosis.

Adolescent↗

Bone sialoprotein mRNA and protein expression in human multiple myeloma cell lines and patients.

Bone sialoprotein (BSP) is a glycoprotein essentially found in mineralizing connective tissues. We have recently demonstrated that BSP is ectopically expressed by carcinomas that metastasize to bone with high frequency. Multiple myeloma (MM) is characterized by the localization of tumour plasma cells in the bone marrow. In this study, BSP expression was evaluated in human myeloma cell lines and in bone marrow aspirates and one ascites fluid from MM patients. BSP was detectable in conditioned media of MM cell lines. Using FACS analysis and in situ hybridization, we demonstrated that tumour cells from all MM patients and cell lines analysed express BSP at both the protein and the mRNA level.

Bone Marrow↗

Homing behaviour of the malignant cell clone in multiple myeloma.

Multiple myeloma (MM) represents a B cell malignancy characterised by the presence of a monoclonal population of end-stage B cells in the bone marrow. Although fully matured bone marrow plasma cells are the predominant cell type in MM, there is much evidence that also more immature B cells are included in the malignant cell clone which are considered to be the myeloma precursor cells. The fact that these cells are detectable in the blood circulation and that their number increases with disease progression, makes it very likely that they represent the component of the tumour clone that mediates disease dissemination. This implies that these cells must have the potential to extravasate and home to the bone marrow environment. Like the migration mechanisms used by normal leukocytes and/or metastatic tumour cells of non-haematopoietic origin, it can be assumed that this bone marrow homing process is mediated by adhesive interactions and chemotactic signals provided by the microenvironment of the tumour. Once in the bone marrow compartment, myeloma cells will receive the appropriate signals to grow and survive. This aspect of tumour-homing is found to be the result of a functional interplay between the myeloma cells and the surrounding microenvironment, involving the action of several cytokines and adhesion molecules. In the end phase of the disease, myeloma cells can lose their stroma-dependency resulting in extramedullary tumour growth. We review normal B cell homing and discuss molecular mechanisms that determine the homing behaviour of the malignant cell clone in MM.

Animals↗

Immunoglobulin VH gene sequence analysis of spontaneous murine immunoglobulin-secreting B-cell tumours with clinical features of human disease.

The 5T series of multiple myelomas (MM) and Waldenstrsöm's macroglobulinaemia-like lymphomas (WM), which developed spontaneously in ageing mice of the C57BL/KaLwRij strain, shows clinical and biological features that closely resemble their corresponding human diseases. In order to compare the patterns of somatic mutation in VH genes of mouse tumours with those of human counterparts, we have determined and analysed sequences of immunoglobulin VH genes in five cases of murine MM, two of WM and one of biclonal benign monoclonal gammopathy (BMG). Four of five MM and 2/2 WM cases used VH genes of the large J558 family; one MM used a gene of the VGAM3.8 family, and both clones of the BMG used genes of the 36-60 family. N-region insertions were observed in all cases, but D-segment genes were only identified in 6/9 cases, which were all from the D-SP family and translated in reading frame 3. Compared with human MM, in which the VH genes have been found to be consistently hypermutated (mean% +/- SD = 8.8 +/- 3.2), the degree of somatic mutation in the murine tumours was significantly lower (mean% +/- SD = 2.9 +/- 2.3). There was no significant evidence of clustering of replacement mutations in complementarity determining regions (CDR), a feature considered to be characteristic of antigen-selected sequences. However, one clone of the biclonal BMG case showed intraclonal variation, a feature described in some cases of human BMG. These results indicate that murine VH genes in mature tumours differ from human counterparts in the level and distribution of somatic mutations, but support the concept that BMG may be distinct from MM.

Amino Acid Sequence↗

The ubiquitously expressed pICln protein forms homomeric complexes in vitro.

Endothelial cells contain a cell-volume sensitive chloride conductance with biophysical properties similar to those of a ubiquitously expressed chloride current that is activated by cell swelling. The latter current has been associated with the ICln protein (pICln) which may be the chloride channel itself or, alternatively, a channel regulator. We were therefore interested in whether pICln is involved in the endothelial volume-sensitive chloride current. As a first step, we have cloned human pICln and studied its expression at the protein level. Using a polyclonal antiserum raised against human pICln we found a widespread expression of pICln, both in endothelial cells and in other cell lines. A characteristic feature of pICln is its anomalous migration during denaturing polyacrylamide gel electrophoresis. We also demonstrate that bacterially expressed pICln forms homomeric complexes in vitro.

Base Sequence↗

Production of fibronectin and adherence to fibronectin by human myeloma cell lines.

In the present study we examined the production of fibronectin (FN) in 10 human myeloma cell lines (HMCL). By Northern blot analysis we could detect the presence of FN-mRNA in most of these lines. A majority of the cell lines (LP-1, OPM1, SKMM-2, EJM, JJN3 and ARH-77) hybridized with two probes recognizing total FN while the mRNA of one cell line (LB84-1) was shown to hybridize also with a probe recognizing the EDA segment of cellular FN. In one cell line (L363) FN-mRnA could only be detected after PCR amplification. Using an enzyme-linked immunosorbent assay, we could also demonstrate that HMCL secrete FN in their culture medium. Seven myeloma cell lines that produce FN showed a significant adherence to soluble FN. By blocking experiments, this adhesion was found to be mediated by the VLA-4 (alpha 4 beta 1) receptor. The production of fibronectin and the expression of a functional receptor for this protein may represent independent features of myeloma cells but may also be functionally linked. Since fibronectin has recently been identified as a crucial co-factor of IL6 in the regulation of the terminal B cell differentiation, the endogenous FN production may be part of an autocrine-line process mediating the autonomous growth of these cell lines. Alternatively, the FN production may also reflect a mechanism that myeloma cells use to communicate with their natural environment, i.e. the bone marrow stroma.(ABSTRACT TRUNCATED AT 250 WORDS)

Base Sequence↗

[Low flow venous malformations in children].

Low flow venous malformations in children are a diagnostic and therapeutic challenge. They are present at birth but may not be evident; they have a commensurate growth. They are pure or combined (capillary or lymphatic-venous). At examination, one observed soft, compressible bluish swellings; there is no thrill or bruit. They are slow flow anomalies with venous stasis which may induce thrombosis or localized consumptive coagulopathy. Skeletal distortion or bony hypertrophy or hypoplasia may also be observed; histological examination of surgical specimen reveals infiltration of adjacent structures (skin, bone, muscle); ultrasonography and duplex-Doppler may be helpful in differentiating the venous malformation from lymphatic or arteriovenous anomalies. Diagnosis from hemangioma will be obtained by magnetic resonance imaging; this last investigation will also provide informations on the infiltration of the adjacent tissues by the pathologic process. Standard X ray may show phleboliths of skeletal distortion. Most of venous malformations are asymptomatic and treatment consists in reassuring the child and in giving advice to the parents to prevent trauma to the lesion. Conservative treatment must be advocated (compression garments, prevention of thrombosis with salicylates) since total excision of venous malformation is illusory and postoperative morbidity may be important. Surgical excision of limited cumbersome malformations may be indicated; sclerotherapy of the lesion with Ethibloc makes surgery easier.

Arteriovenous Malformations↗