[Cone beam 3D sialography: preliminary study]. / Sialographie 3D en cone beam: étude préliminaire.

INTRODUCTION: Stones, stenosis and inflammatory lesions are the main causes of mealtime syndrome. The aim of paraclinical exam is to find the cause of these obstructive symptoms. Ultrasound is often sufficient to confirm the lithiasic origin of salivary gland swelling. Non-lithiasic salivary obstructions are more difficult to diagnose. We studied the feasibility and quality of a new medical imaging device: three-dimensional (3D) sialography using the technique of cone beam with flat panel (CPCT). PATIENTS AND METHODS: Five patients were included, referred for diagnostic management of non-lithiasic salivary gland parotid colic. It was performed for each patient in the angiography room, conventional sialography and 3D CPCT. Images were compared to conventional sialography. RESULTS: None of catheterization failure or side effects were observed in five patients. 3D CPCT sialography enabled to view gland ducts until their fifth or sixth division. Compared to conventional sialography, 3D CPCT improves signal and contrast to noise ratio. DISCUSSION: This technique allows an anatomic resolution and signal/noise ratio unmatched. It also allows to reduce metallics artefacts. Its main drawback is those associated with ductal catheterization, exposure to ionizing radiation and potential allergy to iodinated contrast agents.

[Thermosensitive sporulation and extracellular serylprotease mutant of B. subtilis]. / Mutant thermosensible de B. subtilis affecté dans la sporulation et la sérylprotéase extracellulaire

Isolation and properties of B. subtilis ts 19 mutant, isolated as thermosensitive for sporulation, are described. At the non permissive temperature (42degreesC), the mutant cells are blocked at stage zero of sporulation and do not excrete extracellular enzymes such as serylprotease and esterase. At the permissive temperature (30degreesC), sporulation and excretion of extracellular enzymes are normal but the serylprotease is modified in its structure. Two molecular forms of this enzyme can be separated by polyacrylamide elecctrophoresis, both more thermolabile than the corresponding enzyme of the mother strain. Experiments of reversion and of transformation for the sporulation character have suggested that ts 19 contained two independent thermosensitive mutations. One of them is responsible for the pleiotropic Spo OA phenotype at the non permissive temperature. The other mutation is likely to reside in the structural gene coding for the extracellular serylprotease and leads to the formation of a modified enzyme which hydrolyzes itself into at least two types of more stable molecules. No conclusion can be drawn with certainty concerning the physiologi-al role of the extracellular serylprotease in sporulation. It may be pointed out however that transformants for the Sp+ character at 42degreesC keep the same impaired serylprotease as the ts 19 mutant and sporulate, at any temperature, as well as the wild strain.

Microevolution through DNA exchange among strains of Neisseria meningitidis isolated during an outbreak in the Czech Republic.

Neisseria meningitidis is a highly variable bacterium. Indeed, N. meningitidis is naturally competent for transformation, and horizontal DNA exchange between strains may lead to mosaic genetic loci in N. meningitidis. We studied such an exchange in nature during an epidemic provoked by N. meningitidis. This epidemic started in the Czech Republic in 1993 and the original epidemic clone was shown to have the antigenic formula (serogroup:serotype:serosubtype) C:2a:P1.2,5. We analysed 145 meningococcal strains isolated in the Czech Republic between 1993 and 1997 using serological and genetic typing methods (multilocus enzyme electrophoresis and polymorphism of pilA and pilD genes). This analysis showed that genetic exchange between epidemic and endemic strains had occurred. Exchanges involved mostly surface-exposed structures such as the capsule, giving rise to new meningococcal variants. The expansion of these variants should be kept under close surveillance.

[Molecular bases of virulence in Neisseria gonorrhoeae]. / Bases moléculaires de la virulence de Neisseria gonorrhoeae.

Gonorrhea remains of clinical concern, due to its frequency, complications, sequelae, increasing prevalence of antibiotic-resistant strains and absence of vaccine. A better understanding of the first stages of infection as well as of mechanisms of escape to immune response appears important. Many pathogenic bacteria express pili on their all surfaces. These structures mediate binding of bacteria to host tissues. Furthermore, gonococcal pili are submitted to a high rate antigenic variation, allowing the escape to host immune response. Pilin antigenic variation occurs by DNA recombination between one of the silent partial variant gene segments and an expressed pilin genes. We have shown that transformation of living bacteria by DNA liberated from lysed cells is a critical strep for antigenic variation. This constitutes the first specific function for a DNA transformation system. Piliation and virulence can change with culture conditions. This observation suggests that pilin expression would be subjected to an adaptative response. We have identified and characterized two genes which act in trans to regulate pilus expression. They determine synthesis of a response regulator and a membrane located sensor. They appear to regulate expression of other genes, possibly also involved in virulence. We present evidence for several environmental factors which may control the degree of piliation.

Breast cancers with round lumps: correlations between imaging and anatomopathology.

A round lump with a well-defined outline is, in most cases, benign. However, in 10 to 20% of all cases, a round and well-defined lump may correspond to a cancer. Most often, it consists of grade III infiltrating ductal carcinoma (IDC). Other histological sub-types may provide round masses with smooth contours: colloid carcinoma (still called mucinous carcinoma), medullary carcinoma, intramammary metastases, intra-cystic papillary carcinoma, lymphoma and high-grade phyllode tumours.

Genetic analysis of a meningococcal population based on polymorphism of the pilA-pilB locus: a molecular approach for meningococcal epidemiology.

The genetic relationships between 88 meningococcal strains were analyzed by using the polymorphism of the pilA gene and the multilocus enzyme electrophoresis. While a good agreement was observed, correlation with antigenic formula (serogroup, serotype, and serosubtype) was incomplete. The inadequacy of serological classification alone in outbreak surveillance may be overcome by DNA-based approaches.

Role of pilA, an essential regulatory gene of Neisseria gonorrhoeae, in the stress response.

Sequence analysis has shown that PilA, a transcriptional regulator of pilin gene expression in Neisseria gonorrhoeae, has extensive homology with the 54-kDa protein of the signal recognition particle of eukaryotes and its receptor, as well as with two proteins of Escherichia coli, FtsY and Ffh, which have been proposed to be a part of a signal recognition particle-like apparatus. We tested the putative role of PilA in protein export in N. gonorrhoeae and did not find any effect. However, we did observe induction of a heat shock response and a previously described slow-growth phenotype when PilA function was impaired. We also examined the interference of pilA expression in E. coli with the function of the products of ftsY and ffh and observed an accumulation of pre-beta-lactamase. We argue against a direct role for PilA in protein export in gonococci and propose instead that PilA is involved in the modulation of cell growth rate in response to different environmental conditions.

Pilus-mediated adhesion of Neisseria meningitidis: the essential role of cell contact-dependent transcriptional upregulation of the PilC1 protein.

Pilus-mediated adherence makes an essential contribution to the pathogenesis of Neisseria meningitidis by allowing the initial localized adherence. Pili are assembled from a protein subunit called pilin. Two proteins, PilC1 and PilC2, are also key elements in the formation of pili as the production of at least one PilC protein is required for pilus assembly. In addition, PilC1 but not PilC2 modulates adhesiveness, most probably by being the adhesin. Recently, both genes have been demonstrated to be controlled by different promoters, pilC2 is expressed from a single transcription starting point (TSP), whereas pilC1 has three TSPs. One of these, PC1.1, corresponds to the unique TSP of pilC2, and two others, PC1.2 and PC1.3, are located in a region upstream of pilC1 but not pilC2. This suggests that both genes may be under the control of separate regulatory pathways. In this work, by engineering pilC1-lacZ and pilC2-lacZ transcriptional fusions, we provide evidence that expression of pilC1, but not that of pilC2, is transiently induced by bacterial cell contact. This induction required viable cells, did not need the presence of pili and relied on the expression of pilC1 from PC1.3. Destruction of this TSP by site-directed mutagenesis did not significantly diminish the piliation level or the basal expression of PilC1, but led to the loss of cell contact-dependent upregulation of pilC1 and to a dramatic decrease in bacterial adhesiveness. Taken together, these data demonstrate that cell contact-dependent upregulation of the transcription of pilC1 at PC1.3 is essential for meningococcal pilus-mediated adhesion.

Intimate adhesion of Neisseria meningitidis to human epithelial cells is under the control of the crgA gene, a novel LysR-type transcriptional regulator.

PilC1, a pilus-associated protein in Neisseria menin- gitidis, is a key element in initial meningococcal adhesion to target cells. A promoter element (CREN, contact regulatory element of Neisseria) is responsible for the transient induction of this gene upon cell contact. crgA (contact-regulated gene A) encodes a transcriptional regulator whose expression is also induced upon cell contact from a promoter region similar to the CREN of pilC1. CrgA shows significant sequence homologies to LysR-type transcriptional regulators. Its inactivation in meningococci provokes a dramatic reduction in bacterial adhesion to epithelial cells. Moreover, this mutant is unable to undergo intimate adhesion to epithelial cells or to provoke effacing of microvilli on infected cells. Purified CrgA is able to bind to pilC1 and crgA promoters, and CrgA seems to repress the expression of pilC1 and crgA. Our results support a dynamic model of bacteria-cell interaction involving a network of regulators acting in cascade. CrgA could be an intermediate regulator in such a network.

Agrobacterium rhizogenes pRi8196 T-DNA: mapping and DNA sequence of functions involved in mannopine synthesis and hairy root differentiation.

This paper presents the map and DNA sequence analysis of pRi8196 transferred DNA (T-DNA) genes encoding root-inducing and mannopine synthesis functions. A canonical 24-base-pair border repeat as well as two "pseudoborders" are present at the functional right T-DNA border. To the left of this border are homologs of the mas1' and mas2' genes of TR pRiA4. Next to these are five open reading frames (ORFs) homologous to ORFs 10-14 of TL of pRiA4. ORFs 10-12 (rolA, rolB, and rolC) are less related to their pRiA4 homologs than are the other large ORFs analyzed here. In contrast to T-DNA genes of pRiA4, pRi8196 T-DNA ORFs 11 and 12 (rolB and rolC) are sufficient to induce hairy roots on carrot disks.