[Cluster of Pseudomonas aeruginosa in a neurosurgical unit]. / Focolaio epidemico da Pseudomonas aeruginosa in un reparto di neurochirurgia.

Hospital infections caused by Pseudomonas aeruginosa and particulary meningitis appear to be very common in neurosurgical wards and in patients with brain traumas. This study was carried out during the period between 25th October and the 11th December 2000 in a neurosurgical ward of the teaching hospital of the University "Federico II" of Naples. During this period, five patients contracted an infection caused by P. aeruginosa. The microorganisim was found to be responsible for three cases of meningitis and two cases of surgical site infections. The P. aeruginosa isolates responsible for the infections and the "environmental" isolates were subjected to genotypic typing through the analysis of macrorestriction patterns of genomic DNA after XbaI digestion of Pulsed Field Gel Electrophoresis (PFGE). Four clinical isolates and an environmental isolate recovered from an hand washing basin located in the sub-intensive care area showed an identical PFGE pattern, as well as the some multiresistant antibiotype. The results of this study allows us to point out that the surveillance programs of infections in hospitals should include the molecular typing of micro-organisms singled out in clinical samples and, in case of outbreaks, also the typing of microorganisms originating from the environment and the hospital staff.

[Genomic typing techniques in a case of skin infection epidemic by Staphylococcus aureus in a newborn unit]. / Utilizzo delle tecniche di tipizzazione genotipica in un focolaio epidemico da Stafilococco aureo in un reparto di neonatologia.

In the present study it has been attempted to characterize the source, the reservoir and the modality of transmission of a skin infection epidemic by Staphylococcus aureus in a Newborn Unit. Every S. aureus isolate from clinician and environmental samples has been submitted to phenotypic typing, by means of antibiotic resistance patterns. The genotype has been analyzed using genomic DNA profile of restriction with Sma I and Pulsed Field Gel Electrophoresis (PFGE). In bacterial infections the epidemiologist nexus can think demonstrated when the stocks isolate from various cases belong to the same one clone. In the Newborn Unit the same one clone of S. aureus has been found on 2 health care workers, on 13 staff bearers characterized, and skin of 5 ill newborn infants. Therefore it has been able to go back to the probable source of infection and to take the right measures.

Glial cell line-derived neutrotrophic factor and neurturin can act as paracrine growth factors stimulating DNA synthesis of Ret-expressing spermatogonia.

Glial cell line-derived neurotrophic factor (GDNF) and neurturin (NTN) are related growth factors which exert trophic effects on several neuronal populations and developing kidney. GDNF-family ligands interact with membrane receptors designated GFRalphas which, in turn, mediate stimulation of the Ret receptor tyrosine kinase. Here we show that Ret, GFRalpha-1 (the GDNF receptor), and GFRalpha-2 (the NTN receptor) are expressed by testicular germ cells, while GDNF and NTN are expressed by Sertoli cells. Both GDNF and NTN stimulate DNA synthesis in spermatogonia. Furthermore, Ret, ligands and co-receptors are expressed in germ cell tumors. Thus, GDNF-family ligands may act as paracrine factors in spermatogenesis and this circuit may be active in germ cell tumors.

Identification of a novel subtype of H4-RET rearrangement in a thyroid papillary carcinoma and lymph node metastasis.

RET/PTC chimeric oncogenes are generated by the fusion of heterologous genes to the RET tyrosine kinase encoding domain. These rearrangements are typical of papillary thyroid carcinomas. RET/PTC1 is one of the most frequently found RET/PTC version and, in all the cases so far reported, it is invariably generated by the fusion of the first encoding exon of the H4 gene to the RET kinase encoding domain. This results in the generation of an oncogenic protein containing the first 101 residues of the H4 protein at the N-terminus. We report the isolation of a novel subtype of H4-RET fusion, designated RET/PTC1L, from a human papillary carcinoma of the thyroid and lymph node metastasis. At variance with the classic one, this novel rearrangement generates a protein containing the N-terminal 150 residues of H4. RET/PTC1L is able to transform NIH 3T3 cells; its transforming ability, however, is 5-fold lower than that of the classic RET/PTC1 isoform. We propose that RET/PTC1L is a novel chimeric oncogene involved in thyroid tumorigenesis; its low transforming ability may be one of the reasons explaining the low frequency by which it is found in human thyroid carcinomas.

TPA induces a block of differentiation and increases the susceptibility to neoplastic transformation of a rat thyroid epithelial cell line.

The PC Cl 3 cell line is a well-characterized epithelial cell line of rat thyroid origin. This cell line retains in vitro the typical markers of thyroid differentiation: thyroglobulin (TG) synthesis and secretion, iodide uptake, thyroperoxidase (TPO) expression, and dependency on TSH for growth. Although the differentiated phenotype of thyroid cells has been relatively well described, the molecular mechanisms that regulate both differentiation and neoplastic transformation of thyroid cells still need to be investigated in detail. Protein kinase C (PKC), the target of tetradecanoylphorbol acetate (TPA), regulates growth and differentiation of several cell types. Here we show that treatment of PC Cl 3 cells with TPA induces an acute block of thyroid differentiation. TPA-treated PC Cl 3 cells are unable to trap iodide and the expression levels of thyroglobulin, TSH receptor, and TPO genes are drastically reduced by TPA treatment. This differentiation block is not caused by a reduced expression of one of the master genes of thyroid differentiation, the thyroid transcription factor 1 (TTF-1). TPA-treated PC Cl 3 cells display an increased growth rate indicating that, in addition to the differentiation block, TPA also significantly affects the growth regulation of thyroid cells. Finally, TPA treatment dramatically increases the number of transformation foci induced in PC Cl 3 cells by retroviruses carrying v-Ki-ras, v-Ha-ras, and v-mos oncogenes. These findings support the notion that the PKC pathway can influence proliferation, differentiation, and neoplastic transformation of thyroid cells in culture.