Ectopic parotid: case report.

A recent case led the authors to re-examine the clinical characteristics of the cervical ectopia of the major salivary glands. These glands develop in the embryo between the sixth and seventh week, starting with the formation of endodermal invaginations of the branchial section of the floor of the primitive mouth. These cell cords, initially solid, proliferate in the underlying mesenchyme, starting from the opening of the future excretory duct, and subsequently branch and canalize. During embryogenesis, the endodermal invaginations become closely interconnected with the adjacent lymphatic tissue. It is thus possible for lymphoid tissue to migrate into the parotid or the other major salivary glands, or conversely, for salivary tissue to become included in the cervical lymph nodes. Very rarely, ectopic salivary gland tissue can also be found in other unusual locations, including the neck region, as a result of a developmental abnormality of the branchial apparatus. The base of the neck is the most common location, while ectopia of the mid third of the neck is quite rare. The authors discuss the clinical details and diagnostic procedure leading to preoperative diagnosis. This congenital anomaly can, albeit rarely, degenerate into cancer, and surgical excision is thus imperative.

Effects of magnesium sulphate on leptin-dependent platelet aggregation: an ex vivo study.

Magnesium sulphate has well known antiplatelet properties. Its effect on leptin-dependent platelet aggregation has not been studied previously. Thus, we performed this ex vivo study to investigate whether magnesium sulphate is able to inhibit leptin-dependent aggregation of human platelets. We obtained platelet rich plasma (PRP) from venous blood samples of 16 healthy male volunteers, and we measured ADP-induced platelet aggregation in the presence of leptin alone (5-500 ng/mL) or leptin and magnesium sulphate (0.25-8 mM). Platelet pre-incubation with leptin led to a significant and dose-dependent increase in ADP-induced platelet aggregation. Magnesium sulphate was able to inhibit the pro-aggregating effect of leptin in a dose-dependent manner. The inhibitory effect was apparent at 1 mM of magnesium sulphate concentration (% maximal aggregation=38.1 +/- 12.2) and reached its maximum at 8 mM (% maximal aggregation=20.0 +/- 7.8). Our results demonstrate that leptin-dependent platelet aggregation is inhibited by magnesium sulphate in a dose-dependent manner. It seems conceivable that the blocking of hydrolysis of phosphoinositide and of intracellular calcium mobilization by magnesium sulphate may be involved in these findings.