Leptin is produced predominantly in adipose tissue but has recently also been found in gastric mucosa. It has been shown that the oral application of leptin induces neuronal activity in the brain stem of rodents. The objective of the present study was to identify this hormone in human saliva and to examine the production and stability of salivary leptin. We have demonstrated production of leptin in salivary glands and oral mucosa by RT-PCR, its storage by immunocytochemistry, and the release of the peptide by RIA . Chromatographic analysis and immunoblotting confirmed the identity of leptin. There is a strong linear correlation (r 2 ‫؍‬ 0.78) between leptin concentrations from simultaneously collected saliva and plasma samples (n ‫؍‬ 61). Stimulation of saliva flow increases total leptin secretion up to 3-fold (P < 0.001). As to the stability of leptin in gastric fluid, we found the peptide was not degraded above pH 3. S INCE THE DISCOVERY of leptin in 1994, research activities have been directed at understanding the regulation and actions of this peptide hormone. Leptin is the product of the obese gene with a single-chain structure and a molecular mass of 16 kDa. It is produced by differentiated adipocytes (1, 2) as well as in the placenta (3, 4). More recently, storage and secretion of leptin has also been demonstrated in the stomach (5-7). The signal function of leptin on the central nervous system has been the major area of research (8 -12). Leptin influences food intake (e.g. by suppressing neuropeptide Y in the hypothalamus [11], and stimulates energy expenditure and thermogenesis (e.g., by interaction with the adrenal cortex [13,14]). However, specific receptors for leptin have been found ubiquitously in the body (e.g., thyroid gland, adrenal glands, lung, placenta, kidney, liver, and endothelial cells [15][16][17]). This suggests a peripheral role for leptin. Interestingly, a specific leptin receptor was recently identified in the gastric mucosa (6) and in other parts of the gastrointestinal tract (18). To date, the sources of leptin as a gastrointestinal receptor ligand have been only partially investigated.It was therefore an objective of the present study to identify and characterize the presence of leptin in saliva. A second aim was to investigate the regulation of leptin in the salivary glands and its stability under gastric conditions. Materials and Methods Sample materialPlasma and saliva were collected simultaneously from healthy adult males (n ϭ 23; age 28 -80 yr; body mass index [BMI] 20 -50 kg/m 2 ) and females (n ϭ 25; age 22-85 yr; BMI 19.5-54 kg/m 2 ) and healthy adolescents (male: n ϭ 13; female: n ϭ 5; age 10 -18 yr; BMI: 15-39.9 kg/m 2 ) recruited in our hospital, who gave informed consent of participation. None of the volunteers took medication or contraceptives and all participants had fasted for at least 2 h. The study was approved by the Ethics Review Board of the University of Erlangen.Plasma was collected with S-Monovettes, saliva was collected with the Salivette device (both Sarst...

The effect of aerosolized perfluorocarbon (PFC) (FC77) on pulmonary gas exchange and lung mechanics was studied in a surfactant depleted piglet model. Sixty minutes after induction of lung injury by bronchoalveolar lavage, 20 piglets were randomized to receive aerosolized PFC (Aerosol-PFC, 10 ml/kg/h, n = 5), partial liquid ventilation (PLV) at FRC capacity volume (FRC-PLV, 30 ml/kg, n = 5) or low volume (LV-PLV, 10 ml/kg/h, n = 5), or intermittent mandatory ventilation (IMV) (Control, n = 5). After 2 h, perfluorocarbon application was stopped and IMV was continued for 6 h. Sixty minutes after the onset of therapy, PaO2 was significantly higher and PaCO2 was significantly lower in the Aerosol-PFC and the FRC-PLV groups than in the LV-PLV and the Control groups; p < 0.001. Six hours after treatment, maximum PaO2 was found in the Aerosol-PFC group: 406.4 +/- 26.9 mm Hg, FRC-PLV: 217.3 +/- 50.5 mm Hg, LV-PLV: 96.3 +/- 18.9 mm Hg, Control: 67.6 +/- 8.4 mm Hg; p < 0.001. PaCO2 was lowest in the Aerosol-PFC group: 24.2 +/- 1.7 mm Hg, FRC-PLV: 35.9 +/- 2.8 mm Hg, LV-PLV: 56.7 +/- 12.4 mm Hg, Control: 60.6 +/- 5.1 mm Hg; p < 0.01. Dynamic compliance (C20/c) was highest in the Aerosol-PFC group; p < 0.01. Aerosolized perfluorocarbon improved pulmonary gas exchange and lung mechanics as effectively as PLV did in surfactant-depleted piglets, and the improvement was sustained longer.

Background: During human pregnancy, 11b-hydroxysteroid dehydrogenase type 2 (11b-HSD2) plays an important role in protecting the fetus from high maternal glucocorticoid concentrations by converting cortisol to inactive cortisone. Furthermore, 11b-HSD2 is indirectly involved in the regulation of the prostaglandin inactivating enzyme 15-hydroxyprostaglandin dehydrogenase (PGDH), because cortisol reduces the gene expression and enzyme activity of PGDH in human placental cells. Objective: To examine developmental changes in placental 11b -HSD2 and PGDH gene expression during the 2nd and 3rd trimesters of human pregnancies. Methods: In placental tissue taken from 20 healthy women with normal pregnancy and 20 placentas of 17 mothers giving birth to premature babies, 11b-HSD2 and PGDH mRNA expression was determined using quantitative real-time PCR. Results: Placental mRNA expression of 11b-HSD2 and PGDH increased signi®cantly with gestational age r 0X55Y P 0X0002 and r 0X42Y P 0X007X In addition, there was a signi®cant correlation between the two enzymes r 0X58Y P , 0X0001X Conclusions: In the course of pregnancy there is an increase in 11b-HSD2 and PGDH mRNA expression in human placental tissue. This adaptation of 11b-HSD2 prevents increasing maternal cortisol concentrations from transplacental passage and is exerted at the gene level. 11b-HSD2 upregulation may also lead to an increase in PGDH mRNA concentrations that, until term, possibly delays myometrial contractions induced by prostaglandins.

Background: On clinical grounds, arachnoid cysts are usually associated with neurological dysfunction. There is little information concerning their involvement in endocrinological disorders. Patients: The experience in 6 children (birth to 12 years) with hypothalamic-pituitary disturbances secondary to the presence of intracranial arachnoid cysts is reported and the literature is reviewed. Results: Three of our children were diagnosed with isolated hormone abnormalities (2 children with precocious puberty and 1 child with growth hormone, GH deficiency). One child presented the unusual combination of GH deficiency and precocious puberty. The remaining 2 children developed panhypopituitarism associated with diabetes insipidus. Conclusion: Arachnoid cysts may cause a wide spectrum of endocrinological disorders. Periodical and complete follow-up of every patient is recommended.

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