Understanding the Second Victim Phenomenon Among Healthcare Workers in an Italian Hospital.

Second victim syndrome (SVS) refers to the psychological trauma experienced by healthcare workers (HCWs) as a result of being involved in an adverse event (AE). Research on the prevalence of SVS and the support needed for HCWs who experience it is limited. A cross-sectional study was conducted at the Health Local Unit of Lecce, in Puglia, to identify the phenomenon of SVS among HCWs and recognize the forms of support received and desired.

Endogenous codeine and morphine in anorexia and bulimia nervosa.

The endogenous plasma alkaloids codeine and morphine were shown to be elevated in patients with anorexia nervosa and bulimia nervosa compared to control subjects. The role of these opioids in the pathophysiology of these eating disorders is discussed in relation to an auto-addiction opioid model. This model proposes that endogenous opioids are released during an initial period of dieting and reinforce a state of starvation dependence [1,2].

High-dose naltrexone and liver function safety.

Studies have found naltrexone useful in the treatment of diseases other than opiate addiction in which endogenous opioids presumably play a role, such as alcoholism and eating disorders. Some of these studies involve high doses (100-200 mg bid). Because investigational studies with high doses (300 mg/day) reported clinically significant increases in liver enzyme levels, the authors measured a spectrum of liver function parameters in response to high doses of naltrexone in a double-blind, crossover trial (100 mg bid) followed by an open-label period (200 mg bid).

Male/female comparison of morphine effect on food intake--relation to anorexia nervosa.

We have proposed that endogenous opioids play a critical role in the etiology of anorexia nervosa by mediating an auto-addiction. A biological predisposition may result from an atypical endogenous opioid system. Morphine activation of the system increases food intake in most species, including normal humans and rats, but decreases food intake in mice.

A detailed longitudinal analysis on the use of naltrexone in the treatment of bulimia.

In accord with our auto-addiction opioid model, naltrexone was previously reported to be effective in the treatment of bulimia in a controlled double-blind clinical trial with a randomized cross-over design. This is a detailed longitudinal analysis over a 16 month period of one subject from that study. Attenuation in bulimic symptoms in two-drug as compared to no-drug periods was demonstrated.

Naltrexone use in the treatment of anorexia nervosa and bulimia nervosa.

Our auto-addiction model suggests that opiate blockade may be therapeutically useful in anorexia nervosa and bulimia nervosa. Naltrexone was administered to out-patient subjects in double-blind clinical trials with randomized cross-over designs. Reduction in binge-purge symptomatology was evident in the naltrexone period over placebo for 18 out of 19 subjects with either bulimia or anorexia nervosa of the bulimic subtype.

Binge eating disorder: response to naltrexone.

Binge eating disorder (BED) is characterized by a bulimic binge eating pattern without the compensatory behaviors of purging or laxative abuse. It is often associated with obesity. The treatment response characteristics are more like bulimia than other forms of obesity.

Effects of U50,488, a selective kappa agonist, on atypical mouse opiate systems.

We have proposed that endogenous opioids play a critical role in the etiology of anorexia nervosa, mediating an auto-addiction, and that atypical opioid systems in mice may be representative of those in anorexia nervosa patients, in contrast to normal humans and rats. A biological predisposition to eating disorders may result from these atypical opioid systems. Definition of these systems as atypical is based on their responses to morphine, which are preferential for the mu receptor subtype.

Atypical endogenous opioid systems in mice in relation to an auto-addiction opioid model of anorexia nervosa.

We have proposed that the atypical opioid system in the mouse may be representative of that in the anorexia nervosa patient and may account for a biological predisposition to the disorder. This is in the context of our auto-addiction model of anorexia nervosa in which endogenous opioids play a critical role in its etiology. Morphine activation of the endogenous opioid systems increases food intake and causes sedation in most species, including normal humans and rats.

Atypical responses to morphine in mice: a possible relationship to anorexia nervosa?

According to our previously proposed auto-addiction hypothesis of chronic anorexia nervosa, patients become addicted to an initial period of dieting through endogenous opioid mediated mechanisms. Morphine causes hyperactivity and anorexia in the mouse, symptoms of anorexia nervosa but responses opposite to those of most species including rats and normal human subjects. This suggests that the atypical opioid systems in the mouse may resemble those of the chronic anorexia nervosa patient in contrast to those of most species including the normal human.

Effects of thioglucoses on sensitivity to insulin hypoglycemic convulsions.

Based on the effects of gold thioglucose (GTG), we have previously proposed a regulatory center in brain which adjusts the convulsive response to insulin hypoglycemia. The sensitivity to insulin hypoglycemic convulsions is decreased 24 hr and increased 1 week after a single i.p.

Thioglucose interactions with a "gold thioglucose-lesioned glucostat".

Our previous studies suggest a central nervous system regulatory center that adjusts the brain's convulsive response to the insulin hypoglycemia based on decreased sensitivity to insulin hypoglycemic convulsions 24 hr after a single i.p. injection of gold thioglucose (GTG).

Effects of bipiperidyl mustard (BPM) lesions on insulin hypoglycemic convulsions.

Systemic gold thioglucose (GTG) is well known to produce hyperphagia, resulting in obesity, and histological damage focused relatively selectively in the ventromedial hypothalamus (VMH). Although structurally very different, bipiperidyl mustard (BPM) produces apparently similar effects. However, a proposed mechanism for concentration and hence localization of GTG toxicity depends on its structural similarity to glucose, binding it to glucoreceptors and focusing the cytotoxicity of the gold thio-portion.

Blood glucose profiles in surgically prepared flaxedilized and anesthetized rats.

Blood glucose profiles were monitored over an extended period of time in surgical rat preparations which included femoral artery and vein cannulations, tracheotomy, carotid artery cannulation and a craniotomy to expose the brain. Rats were under pentobarbital anesthesia, urethane anesthesia or Flaxedil neuromuscular blockage and local anesthesia, Fasted and unfasted rats were compared. These profiles are a foundation for studies of the central nervous system control of feeding behavior and metabolic homeostasis and of hypothalamic glucoreceptors, for which knowledge of the baseline blood glucose profile is particularly important.

Change in sensitivity to insulin hypoglycemic convulsions after gold thioglucose treatment: time course of development.

The sensitivity to insulin hypoglycemic convulsions has been shown to decrease at early times (16 and 24 hr) and increase at later times (1 week) after gold thioglucose (GTG) treatment. Systemically administered GTG is well known to produce hyperphagia, resulting in obesity, and cytological damage focused relatively selectively in the ventromedial hypothalamic area (VMH). Both of these effects on insulin hypoglycemic convulsions occur before the weight gain, but at a time when histological damage visible with cresyl violet stain has already appeared.

Effects of prostaglandin F2alpha on cerebral cortical evoked potentials.

The cerebral cortical action of prostaglandin F2alpha (PGF2alpha) has been determined by recording the effects of intracarotid injections of PGF2alpha on cerebral evoked potentials. PGF2alpha differentially reduced cortical evoked potentials. The cortical action of PGF2alpha appeared to be qualitatively identical with that of norepinephrine (NE) but weaker.

Intracellular recording of cerebral cortical actions of prostaglandins F2alpha (PGF2alpha).

Our reported data on the cortical inhibitory actions of prostaglandin F2alpha (PGF2alpha) and the diversity of data in the literature on cerebral PG actions are examined here in the light of intracellular recording which provides the requisite membrane data for the first time. Thus, 1) intracellular recording from the cat cerebral cortex is obtained for the actions of PGF2alpha and for norepinephrine (NE) and serotonin (5HT). 2) The parallel changes in firing and polarization and the simultaneous transmembrane conductance changes are qualitatively identical for PGF2alpha, NE and 5HT.