We have evaluated the plasma GH response to a single injection of 1 microgram/kg of GH-releasing hormone (GHRH)-40 in 15 obese children and 15 age-matched control children. Most of the obese children showed a subnormal plasma GH response to GHRH and the mean plasma GH integrated area (IC-GH) following stimulation was significantly smaller in obese than control children. Plasma somatomedin-C (SM-C) levels were significantly higher in obese than control children, and were negatively correlated with the peak plasma GH levels (r = -0.616, P less than 0.01) and the IC-GH (r = -0.554, P less than 0.02) after GHRH. Non-esterified fatty acids (NEFA) and fasting plasma insulin levels were also elevated in obese children, but did not correlate with the extent of plasma GH response to GHRH. These data confirm previous observations on the refractoriness of obese children to release GH after GHRH, and imply that it may be due to the feedback inhibition operated by the elevated plasma levels of SM-C.
The large-scale deployment of modern phishing attacks relies on the automatic exploitation of vulnerable websites in the wild, to maximize profit while hindering attack traceability, detection and blacklisting. To the best of our knowledge, this is the first work that specifically leverages this adversarial behavior for detection purposes. We show that phishing webpages can be accurately detected by highlighting HTML code and visual differences with respect to other (legitimate) pages hosted within a compromised website. Our system, named DeltaPhish, can be installed as part of a web application firewall, to detect the presence of anomalous content on a website after compromise, and eventually prevent access to it. DeltaPhish is also robust against adversarial attempts in which the HTML code of the phishing page is carefully manipulated to evade detection. We empirically evaluate it on more than 5,500 webpages collected in the wild from compromised websites, showing that it is capable of detecting more than 99% of phishing webpages, while only misclassifying less than 1% of legitimate pages. We further show that the detection rate remains higher than 70% even under very sophisticated attacks carefully designed to evade our system.
Plasma levels of gonadotropins, PRL, T4, and adrenal and gonadal steroids were measured in two groups of 7- to 9-yr-old and 10- to 11-yr-old obese prepubertal girls, and were compared to those found in groups of nonobese girls of the same age. The data found in normal weight subjects confirm the data reported in the literature, showing a significant rise between the 7- to 9- and 10- to 11-yr groups, of FSH, pregnenolone, dehydroepiandrosterone, testosterone, and estradiol plasma levels, while LH, PRL, T4, cortisol, progesterone, 17-hydroxyprogesterone (17P), and androstenedione remained constant. In the obese subjects, pregnenolone and dehydroepiandrosterone levels are notably higher than in the normal girls, in the same range as those found in adult women; furthermore, they show no rise between the two age groups. The obese prepubertal groups had significantly higher progesterone, androstenedione, and PRL levels in comparison with those observed in girls of normal weight, but 17-hydroxyprogesterone, cortisol, testosterone, LH, and T4 were similar in both groups. Estradiol levels were markedly depressed in the obese girls; FSH levels were higher in the younger girls than in normal subjects. These data indicate that in prepubertal obesity, maturation of adrenal gland function (chiefly the delta 5 pathway), is notably enhanced, whereas gonadal secretion of estradiol is impaired in the presence of high levels of FSH and PRL.
The adrenal steroid secretion was studied in 6 prepubertal obese boys and 6 obese boys at the first stage of sexual maturation according to Tanner. Twelve normal boys, closely matched for age and stage of sexual maturation, were also studied as controls. Pregnenolone and dehydroepiandrosterone plasma levels were found to be significantly (P less than 0.001) higher in both groups when compared with normal boys. All the values, apart from pregnenolone in the prepubertal group, returned to normal after weight loss. Progesterone was found significantly increased (P less than 0.001) in both groups and normal after weight loss. 17-OH-progesterone plasma levels showed no significant difference between the obese and control groups. Androstenedione was increased in the prepubertal group before and normal after weight loss; no significant difference was found in the other group. Testosterone and estradiol showed normal values in the two groups both before and after weight loss. Cortisol showed a similar pattern. It can be concluded that an increased cortico-adrenal activity is present in obese boys as already reported in obese girls. This finding could explain the precocious adrenarche which often occurs in these patients. The increased adrenal androgen secretion might be due to an increased cortico adrenal stimulating hormone secretion or to an enhanced adrenal sensitivity to this hypothetical hormone.
The response of GH to acute administration of GH-releasing hormone (GHRH) was evaluated in 19 patients with thalassemia major and 8 normal children. In 13 of the 19 patients, GHRH induced a definite increase (greater than 5 ng/ml) in plasma GH levels, with peaks occurring 5-45 min postinjection. In 6 patients there was little or no GH rise after GHRH treatment. Overall, the mean GH response to GHRH of patients with thalassemia was lower than that of normal children. These data indicate that in thalassemia major, in addition to the described defect at the hepatic GH receptor or postreceptor level which impedes generation of somatomedins, there may be a marked impairment in somatotroph function. In one patient in whom the GH response to GHRH was superimposable on that of normal subjects, there was a blunted GH response to insulin hypoglycemia. This finding indicates that functional damage in hypothalamic structures for GH control can also occur in thalassemic patients.
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