Evaluation of salivary surface tension in a cohort of young healthy adults.

OBJECTIVE: To determine salivary pH, flow rate (FR) and surface tension (γs) in a cohort of 30 healthy young adults. To acquire cohort biological independent variables (age, gender, weight, height, medications, smoking, pathologies, and allergies) and to correlate them with pH, FR and γs obtained values. Evaluate the possible variation of the γs values during the time after the withdrawal and the influence of the operational abilities of the experimenting operators. Evaluate the relationship between γs, pH and FR  and the dependence between pH and FR. PATIENTS AND METHODS: Non-stimulated saliva samples were taken in four different time span, for three days, with a drooling method for 15 minutes. The saliva sample was analyzed, in terms of γs, by two different operators (OP1 and OP2), twice consecutive (γs-1 and γs-2) for a total of 360 measurements. The γs was calculated using the du Noüy method. The FR was evaluated by weighing technique and pH by pH indicator papers. RESULTS: The measurements of γs performed by two different operators (OP1, OP2) showed respectively average values of 46.46 mN/m and 43.45 mN/m, while the mean FR was 0.29 ± 0.13 mL/min and the average pH was 7.1 ± 0.43. There were no significant correlations between γs and the biological variables analyzed. CONCLUSIONS: We can consider as reference values, in a sample of young adults, γs 45.56 ± 6.51 mN/m.

The isoelectric focusing of human thyroglobulin.

The isoelectric focusing of human thyroglobulin has been studied on slab gels. Three bands, focusing between pH 4.4 and 4.7, are observed. Deglycosylation of thyroglobulin does not affect the distribution of focused bands, but increases the pH range of focusing slightly. Native thyroglobulin and its half-sized subunit show the same distribution of isoelectric bands. Refocusing of one band results in the appearance of the three original bands. It appears that soluble complexes of thyroglobulin with ampholyte account for the apparent heterogeneity observed on isoelectric focusing.

Environmental tobacco smoke exposure in inner-city children.

Exposure to environmental tobacco smoke (ETS) was assessed as part of a pilot study aimed at determining the extent of multiple toxicant exposures in children from inner-city areas of Baltimore, MD. Questionnaire data on sources of ETS and urinary cotinine were obtained in children considered at high risk for urban exposures because of previous or current overexposure to one inner-city environmental hazard, lead. Fifty-three (67.1%) of the 79 participants were exposed to ETS in the preceding 48 h as assessed by questionnaire. Cotinine was present in 77 (98.7%) of the 78 samples assayed with a mean of 79.2 ng/mg creatinine (54.7 ng/ml). Eighty % of children had cotinine values > or = 30 ng/mg creatinine, a level commonly associated with household ETS exposure. Levels in children without reported ETS exposure in their homes were also elevated (mean = 45.0 ng/mg creatinine). As expected, blood lead levels were elevated with a mean of 23.6 micrograms/dl. We conclude that these inner-city children have substantial exposures to both ETS and lead. Furthermore, the presence of elevated cotinine levels in children without known household exposure suggests that ETS should be considered an urban toxicant as well as an individual residential exposure.

Benzene exposure, assessed by urinary trans,trans-muconic acid, in urban children with elevated blood lead levels.

A pilot study was performed to evaluate the feasibility of using trans,trans-muconic acid (MA) as a biomarker of environmental benzene exposure. A secondary aim was to provide data on the extent of exposure to selected toxicants in a unique population consisting of inner-city children who were already overexposed to one urban hazard, lead. Potential sources of benzene were assessed by a questionnaire. Exposure biomarkers included urinary MA and cotinine and blood lead. Mean MA was 176.6 +/- 341.7 ng/mg creatinine in the 79 children who participated. A wide range of values was found with as many as 10.1%, depending on the comparison study, above the highest levels reported in adults not exposed by occupation. Mean MA was increased in children evaluated in the afternoon compared to morning, those at or above the median for time spent playing near the street, and those studied in the first half of the investigation. MA levels were not associated with blood lead or, consistently, with either questionnaire environmental tobacco smoke (ETS) data or cotinine. As expected, the mean blood lead level was elevated (23.6 micrograms/dl). Mean cotinine was also increased at 79.2 ng/mg creatinine. We conclude that the use of MA as a biomarker for environmental benzene exposure is feasible since it was detectable in 72% of subjects with a wide range of values present. In future studies, correlation of MA with personal air sampling in environmental exposure will be essential to fully interpret the significance of these findings. In addition, these inner-city children comprise a high risk group for exposure to environmental toxicants including ETS, lead, and probably benzene, based on questionnaire sources and its presence in ETS.

Abnormal serotonergic control of prolactin and cortisol secretion in patients with seasonal affective disorder.

The effects of the serotonergic agent d,l-fenfluramine (60 mg PO) or a placebo on serum prolactin (PRL) and cortisol levels were evaluated in seven patients (five men and two women) with seasonal affective disorders (SAD) and in eight normal controls (eight men and two women). Both groups were tested in fall/winter when patients with SAD suffered depressive symptoms and in spring/summer, when patients were euthymic. Spring/summer and fall/winter tests gave similar results. PRL and cortisol patterns were similar in all subjects after placebo, whereas both hormonal responses to d,l-fenfluramine were significantly lower in patients with SAD than in normal controls. Correlation studies between the two hormonal responses revealed that on both periods the amplitudes of PRL and cortisol increments were significantly and positively correlated in patients with SAD. These data show diminished serotonergic responsiveness in SAD regardless of the actual depressive status of the patients. They are consistent with a decrease of central serotonergic activity in SAD.

Serotonergic control of TSH and PRL secretion in obese men.

To evaluate whether the inhibitory control of TSH and the stimulatory control of prolactin (PRL) secretion exerted by endogenous serotonin was altered in obesity, 22 obese men and 10 normal controls were tested with TRH (200 micrograms IV bolus) in the presence (experimental test) and absence (control test) of the serotonergic agonist fenfluramine (60 mg PO 90 min before TRH). Control and experimental tests were also performed in seven male patients with subclinical hypothyroidism and were repeated in the same obese subjects after substantial weight loss. Basal TSH levels were similar in control and obese men. Normal TSH responses to TRH (peak less than or equal to 14 mU/L) were observed in all normal controls (mean peak +/- SE 9.8 +/- 0.6 mU/L). In contrast, obese men were divided into two groups: nine in whom the TRH-induced TSH rise was higher than normal (group I: mean peak = 16.5 +/- 0.5 mU/L) and 13 in whom it was normal (group II: mean peak = 10.6 +/- 0.7 mU/L). The hypothyroid men all had elevated basal and TRH-stimulated TSH levels. Basal PRL concentrations were similar in the normal controls and both groups of obese subjects. The PRL response to TRH was lower in both group I and group II obese men than in normal controls and was similar between group I and group II.(ABSTRACT TRUNCATED AT 250 WORDS)

p27: a potential main inhibitor of cell proliferation in digestive endocrine tumors but not a marker of benign behavior.

The immunohistochemical expression of the inhibitors of cyclin-dependent kinases p21 and p27 was investigated in 109 endocrine tumors of the pancreas and gastrointestinal tract and compared with that of Ki67 and p53. p21 was found to be scarcely expressed without significant differences between benign and malignant or between differentiated and undifferentiated tumors. This suggests no relationship between changes in p21 levels and clinical behavior in these endocrine tumors. p27 was found to be highly expressed in differentiated neoplasms and proved to be inversely related to Ki67 labeling (P =.02), which was usually low. These data indicate that p27 may have an important inhibiting role on the low proliferation rate of the tumors. Moreover, the protein may have a role in the resistance of differentiated endocrine tumors to chemotherapeutic agents. p27 high-expressor neoplasms were frequent in either benign (70.6%) or malignant (81.4%) differentiated tumors, thus not allowing the use of this protein for the differential diagnosis of malignant neoplasms as suggested for endocrine tumors of parathyroid and pituitary. Poorly differentiated endocrine carcinomas, which differred from the differentiated tumors for their very high Ki67 levels and frequent p53 expression, showed low or absent p21 and p27 in most cases. Classical midgut carcinoids were characterized by a sharp discrepancy between malignant behavior and very bland proliferative pattern, with Ki67 and p27 expressions similar to that of benign tumors.

Endogenous opioids modulate the oxytocin response to insulin-induced hypoglycaemia and partially mediate the inhibitory effect of ethanol in man.

Abstract The possible inhibition exerted by ethanol on the oxytocin (OT) response to insulin-induced hypoglycaemia was tested in man. Furthermore, the possibilities that endogenous opioids play a role in the control of hypoglycaemia and/or ethanol action on OT were examined. Insulin tolerance tests were performed in three groups of eight age- and weight-matched normal men treated with: 1) naloxone, group 1 1 mg bolus naloxone + 2.5 mg over 105 min, group 2 2 mg bolus naloxone + 5 mg over 105 min, group 3 4 mg bolus naloxone + 10 mg over 105 min; 2) ethanol (50 ml in 110ml of whiskey) to all the groups; 3) a combination of ethanol + naloxone; 4) normal saline. Furthermore, the effect of ethanol + naloxone (4+10mg) in the absence of insulin-induced hypoglycaemia was evaluated in seven additional subjects. During this latter test, the plasma levels of OT remained unchanged. Insulin-induced hypoglycaemia produced a 2.2-fold increment in plasma OT levels in the control experiments. This response was not changed by the treatment with the lowest dose of naloxone (1+2.5mg) in group 1, but it was significantly enhanced by administration of naloxone at higher doses (mean peak OT levels rose 2.8-fold in both group 2 and group 3). In all subjects the OT response to hypoglycaemia was completely abolished by ethanol. However, when ethanol was given together with naloxone, the hypoglycaemia-induced OT rise was only partially inhibited by ethanol. At all doses naloxone produced similar effects; in fact, in all groups OT rose 1.5-fold in response to hypoglycaemia during insulin tolerance test + ethanol + naloxone. Neither naloxone nor ethanol altered the basal secretion of OT, as tested during 45 min before the insulin tolerance test. These data demonstrate that the OT response to insulin-induced hypoglycaemia is inhibited by ethanol. Furthermore, the data indicate that endogenous opioids are involved in the control of hypoglycaemia-stimulated OT secretion and partially modulate ethanol inhibitory action.

Naloxone decreases the inhibiting effect of ethanol on the release of arginine-vasopressin induced by cigarette smoking in man.

In order to establish whether ethanol exerts its inhibiting effect on the nicotine-induced release of arginine-vasopressin (AVP) by interacting with an opioid pathway, six normal volunteers were treated with naloxone (2 or 4 mg as IV bolus, plus 5 or 10 mg infused over 105 minutes) during (2 nonfilter) cigarette smoking and ethanol (50 mL to 110 mL of whiskey) drinking. In addition, control experiments with naloxone, ethanol, or cigarette smoking alone were performed. When given alone, naloxone and ethanol did not modify AVP secretion, whereas nicotine increased plasma AVP levels by about 2.5-fold. This effect was completely blocked by ethanol. In the presence of naloxone, AVP rose only by about 1.7-fold in response to nicotine. Since naloxone only partially reversed the inhibiting effects of ethanol, only a partial involvement of opioid peptides in ethanol action might be supposed. Alternatively, ethanol and naloxone-sensitive opioids might produce their inhibiting effects on AVP rise in response to nicotine through independent pathways.

Effect of obesity and weight loss on arginine vasopressin response to metoclopramide and nicotine from cigarette smoking.

We have previously reported an impaired arginine vasopressin (AVP) response to insulin-induced hypoglycemia in obese men, suggesting a hypothalamic-posterior pituitary disorder in obesity. In the present study, we examined the AVP response to other releasing stimuli with a central site of action. The AVP response of 10 obese men to metoclopramide (MCP) or nicotine inhaled with cigarette smoking was compared with that obtained in eight sex- and age-matched controls. The AVP increase during nicotine and MCP tests were significantly lower in the obese patients than in the normal controls. Obese men were restudied after substantial weight loss. The AVP response to nicotine and MCP administration was significantly higher than before slimming and did not differ from that observed in the normal weight subjects. These results demonstrate obesity-related alterations in the AVP responsiveness to nicotine inhaled with cigarette smoking and MCP, supporting the hypothesis for a hypothalamic-posterior pituitary disorder in obesity.

Reduced sensitivity to pirenzepine-induced blockade of growth hormone responses to arginine, exercise, and growth hormone-releasing hormone in type I diabetic subjects.

The present study was performed to establish whether the mechanism by which the cholinergic system influences growth hormone (GH) release was altered in type I diabetic patients. Therefore, we investigated in a dose-response fashion the inhibitory effect of the muscarinic cholinergic receptor antagonist pirenzepine on the GH responses to arginine infusion (30 g infused intravenously (IV) in 30 minutes), exercise (bicycle ergometer test at an intensity of 75 W for 30 minutes), or 1-44 GH-releasing hormone (GHRH) (1 microgram/kg in an IV bolus). In a preliminary study, IV injection of 17.5 mg pirenzepine failed to produce modification in the GH response to arginine infusion in both diabetic (N = 4) and normal subjects (N = 4), and to exercise (diabetics, N = 4; normals, N = 4). Therefore, other subjects were tested without and with 20, 25, and 30 mg pirenzepine during arginine (diabetics, N = 7; normals, N = 7) or exercise (diabetics, N = 7; normals, N = 7) tests. Each subject was tested four times. Diabetic patients presented higher GH responses to stimulation with arginine or exercise than normal controls. In both groups, pirenzepine administered at doses ranging from 20 to 30 mg produced a dose-related inhibition of the GH response to arginine and exercise, which was almost complete when 30 mg pirenzepine was administered. However, the percent inhibition produced by 20 or 25 mg pirenzepine in the arginine test and by 20 mg in the exercise test was significantly lower in the diabetic patients than in the normal controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of thyroid status on the paradoxical growth hormone response to thyrotropin-releasing hormone in human obesity.

Thyrotropin-releasing hormone (TRH) tests were performed in 38 age- and weight-matched obese but otherwise healthy men. In all subjects, total thyroxine (T4) and triiodothyronine (T3) concentrations were in the normal range. According to basal and TRH-stimulated serum thyrotropin (TSH) levels, subjects were divided into the following three groups: group I (n = 14), euthyroid subjects; group II (n = 11), euthyroid subjects with normal basal but abnormally elevated TSH responses to TRH; group III (n = 13), subjects with elevated basal and TRH-induced TSH levels (subclinical hypothyroidism). Basal TSH levels were 1.8 +/- 0.4 mU/L in group I, 1.7 +/- 0.3 in group II, and 6.0 +/- 0.7 in group III. In both groups II and III, TRH-induced TSH increments were above the normal range (maximal increment > 14 mU/L) and were significantly higher than in group I. The definition of euthyroidism for groups I and II and of subclinical hypothyroidism for group III according to the basal levels of TSH was confirmed by clinical (Billewicz index), hormonal (serum free-T4 levels), and metabolic (serum apoprotein [apo] AI levels) parameters. Basal concentrations of growth hormone (GH) were similar in all groups. When GH levels after TRH stimulation were measured, significant increments (peak minus baseline > 5 micrograms/L) were observed in nine of 13 hypothyroid obese men. The overall mean peak GH increase in group III was 4.5 times higher than baseline and was observed at 45 minutes. None of the euthyroid obese subjects of groups I and II showed any significant change in GH levels in response to TRH.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of nitric oxide on basal and TRH-or metoclopramide-stimulated prolactin release in normal men. volpi@ipruniv.cce.unipr.it.

In order to establish whether nitric oxide (NO) is involved in the regulation of basal and/or TRH- or metoclopramide (MCP)-stimulated PRL secretion, normal male subjects were treated i.v. with the NO-synthase (NOS) inhibitor N-nitro-L-arginine methyl ester (L-NAME) (40 mg/kg injected plus 50 mg/kg infused over 60 min) in basal conditions (N.7 subjects) or just before the PRL releasing hormone TRH (20 or 200 microg iv) (N.7 subjects) or the antidopaminergic agent MCP (1 or 10 mg iv) (N.7 subjects). In control experiments, subjects received normal saline instead of L-NAME. The administration of L-NAME modified neither the basal secretion of PRL, nor the PRL release induced by TRH (20 or 200 microg) or MCP (1 or 10 mg). These data suggest that in humans, NO is not involved in the control of PRL release at the anterior pituitary level.

Age-dependent decrease in the growth hormone response to growth hormone-releasing hormone in normally cycling women.

OBJECTIVE: To establish possible changes in GH secretion in normally cycling women with increasing age. DESIGN: Controlled clinical study. PATIENTS: Nine younger (18 to 33 years) and nine older (41 to 46 years) healthy women. SETTING: Tests were performed on the 22d day of regular cycles. INTERVENTION: All subjects were tested with GH-releasing hormone (GH-RH) (1 mg/kg body weight), the acetylcholinesterase inhibitor pyridostigmine (120 mg by mouth), the somatostatin inhibitor arginine (30 g infused IV over a 30-minute period) alone, and the combination of GH-RH plus arginine or GH-RH plus pyridostigmine. MAIN OUTCOME MEASURES: Glucose, cortisol, androgens, estrogens, thyroid hormones, and insulin growth-like factor (IGF-I) were measured in basal samples. Serum GH levels were measured in samples taken before and over a 2-hour period after drug administration. RESULTS: All basal hormonal values were similar in younger and older women. Insulin growth like factor-I levels were lower in older women. The GH responses to GH-RH alone, pyridostigmine alone, or the combination were lower in the older than in the younger group and were correlated negatively with age. In contrast, either arginine alone or GH-RH plus arginine produced similar GH responses in the two groups. CONCLUSION: These data indicate that the cholinergic stimulatory regulation of GH release is reduced in the older cycling women. Because acetylcholine inhibits hypothalamic somatostatin release, the reduced cholinergic tone in other subjects may result in an increased somatostatinergic tone. Normalization in older women of the reduced GH response to GH-RH by arginine supports this hypothesis.

Localization of putative biochemical messengers during Eisenia foetida (Annelida, Oligochaeta) development.

This histochemical-immunohistochemical study was performed on the earthworm Eisenia foetida at different developmental stages, to investigate the presence and distribution of cholinergic molecules (AChE, BuChE, alpha-bungarotoxin-binding sites), several biogenic amines (5HT and catecholamines), and some immunologically-related peptides (somatostatin. FMRF-amide, VIP, substance-P, bombesin). The results showed that the pattern of labelling for the markers is different at different stages. In summary, cholinesterases appeared widely distributed in the early embryonic stages. They then were localized in particular areas of the developing nerve and muscle tissues, whereas in newborn and adult earthworms they were restricted to ventral muscular fibers and to some CNS cells. Biogenic amines were constantly present in the embryonic and adult nervous tissues. Immunologically-related peptides were detectable after organogenesis. Our results provide indirect evidence for a role of cholinesterases in regulating early intercellular communications, neurogenesis and myogenesis, and support the hypothesis that some conservative sequences of messenger peptides arose very early in evolution.

Mucinous cystadenoma of the pancreas as a cause of acute pancreatitis.

Acute pancreatitis is only rarely the first presentation of a cystic neoplasm of the pancreas. Mucinous cystadenomas have not been reported to be a cause of acute pancreatitis; however, we present two cases of mucinous cystadenoma of the pancreas which have caused acute pancreatitis. Both patients (female) presented acute abdominal pain, with serum amylase elevation and ultrasound scan (US) and computed tomography (CT) evidence of moderate pancreatitis, which resolved with medical treatment; fluid collection in the distal pancreas had been misinterpreted as a pseudocyst. There was no history of alcohol abuse or gallstone disease. After distal pancreatectomy the diagnosis of mucinous cystadenoma was confirmed; in one case a large pseudocyst was associated with this diagnosis. Pre-operative differential diagnosis between inflammatory and neoplastic cysts is difficult, especially when the patient's first presentation is due to an episode of acute pancreatitis. A neoplastic cyst should be considered when acute pancreatitis attacks occur in non-alcoholic women, who do not have gallstone disease.

[Microbiological characterization of solid wastes and aerosol in a municipal solid waste landfill site]. / Caratterizzazione microbiologica dei rifiuti solidi e degli aerosol che si generano nelle discariche controllate di rifiuti solidi urbani.

Authors report data about microbiological characterization of solid wastes and aerosol in the municipal solid waste landfill site in Poiatica (RE). In solid waste samples high values of total coliform and fecal coliform were observed (10(5)-10(6) CFU/g): total bacterial counts at 22 degrees, at 36 degrees and at 44 degrees ranged from 10(7) to 10(9) CFU/g. Aerosol samples collected during waste movement in the landfill site showed values of total and fecal bacterial ranging from 10(3)-10(4) CFU/m3. Staphylococci and fungi reported the same values while streptococci, total and fecal coliform and spore evidenced lower values. Municipal solid wastes and aerosol have to be considered as an infective substrate: it is necessary to adopt protective barriers in occupationally exposed subjects.