The effects of fluoride on cell migration, cell proliferation, and cell metabolism in GH4C1 pituitary tumour cells.

The consumption of drinking water rich in fluoride has toxic effects on the central nervous system. In cell biology research, fluoride is currently used as a phosphatase inhibitor. The aim of the present study was to evaluate the effect of fluoride on different physiological processes in GH4C1 pituitary tumour cells. We used a range of different fluoride concentrations, from levels below normal human serum concentrations (0.23 and 1.2 micromol/L) to those observed in chronically exposed persons (10.7 micromol/L) and above (107 and 1072 micromol/L). Treatment of 10.7 micromol/L fluoride resulted in a discrete induction of DNA synthesis, without a change in cell number. Cell migration, a behaviour stimulated by growth factors, was increased in cells treated with 2.4 micromol/L. At this fluoride concentration, changes in phosphorylation status of both cytoskeletal and cytosolic protein fractions, as well as in actin cytoskeletal arrangements were observed. The GH4C1 fluoride treated cells had significantly less cellular protein than control cells, suggesting an effect of fluoride on hormone secretion and protein synthesis in this endocrine cell. The bioreduction of MTT was significantly increased with a wide range of fluoride concentrations. With the highest fluoride concentration, 1072 micromol/L, all of the analysed parameters were significantly reduced, suggesting that this dose is highly toxic in GH4C1 cells. Our results show that biologically relevant concentrations of fluoride are capable of increasing cell migration in tumour cells, suggesting that exposure to fluoride could stimulate tumour invasion.

[American cutaneous leishmaniasis: special features in diagnosis and therapy]. / Kutane amerikanische Leishmaniose - Besonderheiten der Diagnostik und Therapie -

HISTORY AND CLINICAL FINDINGS: Three weeks after returning from a trip to Guatemala, a 33-year-old man developed two ulcers with indurated edges on his right leg and painful lymph nodes in the right groin. His general condition was not impaired. EXAMINATIONS: Histological examination revealed cellular infiltrates of the corium by lymphocytes and plasma cells, always accompanied by epithelial cells and multinuclear giant cells. Special stainings were unable to detect pathogens but Leishmania brasiliensis was identified using PCR. The Leishmania culture remained negative. THERAPY AND COURSE: After 7-day intravenous therapy with 20 mg/kg/d pentostam (pentavalent antimonial compound), the patient developed gastrointestinal complaints, coupled with a marked elevation of transaminases. Therapy was discontinued until the transaminase values normalized, then continued in reduced dosage (12 mg/kg body weight) for 23 days. The ulcers and lymphadenitis healed under this therapy. CONCLUSION: The diagnosis of American cutaneous Leishmaniasis may be complicated by the relative lack of pathogens in the lesions. PCR diagnosis are very helpful here. The therapy must be systemic owing to the danger of progression to mucocutaneous Leishmaniasis. The standard therapeutic pentostam has, however, a high rate of side effects and administration is exclusively intravenous.

Infección congénita por virus herpes simplex / Congenital infection due to herpes simplex virus

Se presentan 5 casos de probable infección herpética intrauterina; en 4 de ellos se comprobó clínicamente la presencia de herpes neonatal, observándose un caso localizado a piel, dos casos de herpes diseminado y un herpes neonatal con compromiso del sistema nervioso central. En los cuatro casos enfermos se descartó la posibilidad de infección postnatal o durante el parto, puesto que presentaron signos o síntomas de la enfermedad antes de transcurrir 24 horas de vida. En ellos se plantea la posibilidad de infección transcervical o transplacentaria. Todos los recién nacidos fueron tratados con aciclovir endovenoso por 10 días, evolucionando bien 3 de ellos; los otros 2 fallecen; uno a los 9 días y el otro a los 2 meses de vida por encefalitis y secuelas neurológicas severas, respectivamente