PubMed Health⌕ Search

Biomedical subjects

H Bergen

Publications and source records attributed to H Bergen.

11 recordsLinked to original sources
PubMed2006

Aggressive behaviour in the high-secure forensic setting: the perceptions of patients.

Twenty-seven patients undergoing treatment in a high-secure forensic facility participated in focus group interviews to elicit their perceptions of (1) the factors leading to aggressive behaviour; and (2) strategies to reduce the risk of such behaviour. The focus group interviews were audiotaped, transcribed and analysed using content analysis. The participants identified that a combination of patient, staff and environmental factors contributed to violence in the study wards. The cause of aggressive behaviour centred around five major themes: the environment; empty days; staff interactions; medication issues; and patient-centred factors. Potential strategies identified by patients to reduce aggressive behaviour included: early intervention; the provision of meaningful activities to reduce boredom; separation of acutely disturbed patients; improved staff attitudes; implementation of effective justice procedures; and a patient advocate to mediate during times of conflict. Findings suggested that social and organizational factors need to be addressed to change the punitive subculture inherent in forensic psychiatric facilities, and to ensure a balance between security and effective therapy.

Aggression↗
PubMed1998

A PHEX gene mutation is responsible for adult-onset vitamin D-resistant hypophosphatemic osteomalacia: evidence that the disorder is not a distinct entity from X-linked hypophosphatemic rickets.

Previous investigators described a kindred with an X-linked dominant form of phosphate wasting in which affected children did not have radiographic evidence of rickets, whereas older individuals were progressively disabled by severe bowing. They proposed that this kindred suffered from a distinct disorder that they referred to as adult-onset vitamin D-resistant hypophosphatemic osteomalacia (AVDRR). We recently identified a gene, PHEX, that is responsible for the disorder X-linked hypophosphatemic rickets. To determine whether AVDRR is a distinct form of phosphate wasting, we searched for PHEX mutations in affected members of the original AVDRR kindred. We found that affected individuals have a missense mutation in PHEX exon 16 that results in an amino acid change from leucine to proline in residue 555. Clinical evaluation of individuals from this family indicates that some of these individuals display classic features of X-linked hypophosphatemic rickets, and we were unable to verify progressive bowing in adults. In light of the variability in the clinical spectrum of X-linked hypophosphatemic rickets and the presence of a PHEX mutation in affected members of this kindred, we conclude that there is only one form of X-linked dominant phosphate wasting.

Adolescent↗
PubMed1996

Obese gene expression: reduction by fasting and stimulation by insulin and glucose in lean mice, and persistent elevation in acquired (diet-induced) and genetic (yellow agouti) obesity.

Mutations in the obese (ob) gene lead to obesity. This gene has been recently cloned, but the factors regulating its expression have not been elucidated. To address the regulation of the ob gene with regard to body weight and nutritional factors, Northern blot analysis was used to assess ob mRNA in adipose tissue from mice [lean, obese due to diet, or genetically (yellow agouti) obese] under different nutritional conditions. ob mRNA was elevated in both forms of obesity, compared to lean controls, correlated with elevations in plasma insulin and body weight, but not plasma glucose. In lean C57BL/6J mice, but not in mice with diet-induced obesity, ob mRNA decreased after a 48-hr fast. Similarly, in lean C57BL/6J controls, but not in obese yellow mice, i.p. glucose injection significantly increased ob mRNA. For up to 30 min after glucose injection, ob mRNA in lean mice significantly correlated with plasma glucose, but not with plasma insulin. In a separate study with only lean mice, ob mRNA was inhibited >90% by fasting, and elevated approximately 2-fold 30 min after i.p. injection of either glucose or insulin. These results suggest that in lean animals glucose and insulin enhance ob gene expression. In contrast to our results in lean mice, in obese animals ob mRNA is elevated and relatively insensitive to nutritional state, possibly due to chronic exposure to elevated plasma insulin and/or glucose.

Animals↗
PubMed1996

Effects of nutritional status and aging on leptin gene expression in mice: importance of glucose.

The factors regulating leptin mRNA under physiological conditions have not been fully elucidated, although both insulin and glucose have been implicated. Since, in male mice, plasma glucose decreases with age without a change in body weight or insulin, aging mice constitute a model to examine effects of glucose independent of effects of insulin or body weight. Therefore, we measured leptin mRNA in adipose tissue of 6-, 15- and 24-month-old C57BL/6J male mice, sacrificed either after a 48 h fast (nutritional deprivation) or 15 min after an intraperitoneal injection of glucose (2 mg/g body weight) (nutritional stimulation). There was a significant effect of both age and nutritional status on leptin mRNA, correlated with effects of age and nutritional status on plasma glucose. Leptin mRNA correlated with body weight, plasma glucose and plasma insulin. After statistically removing effects of plasma glucose, the remaining effects of age, nutritional status, and plasma insulin on leptin mRNA were no longer significant. However, after statistically removing effects of plasma insulin, the remaining effects of age, nutritional status, and plasma glucose continued to be significant. When nutrition-deprived and nutrition-stimulated mice were analyzed separately, plasma glucose significantly correlated with leptin mRNA in both groups, but body weight and plasma insulin correlated with leptin mRNA only in nutrition-deprived mice. When mice at each age were analyzed separately, glucose correlated with leptin mRNA at every age, and after statistical removal of the effects of glucose, the remaining effects of insulin on leptin mRNA were no longer significant at any age. These results support the hypothesis that plasma glucose is important in the regulation of leptin gene expression.

Aging↗
PubMed1992

LHRH neurons: functions and development.

Examination of the properties of developing LHRH neurons, by in situ hybridization procedures or LHRH immunocytochemistry, showed that these cells (1) are unique among neuroendocrine cells in their origin from the epithelium of the medial olfactory pit, and (2) express LHRH mRNA. LHRH neurons, visualized by either method, tended to be clustered when seen along the migration route in the nasal mesenchyme. Neural cell adhesion molecule (NCAM) is present on the central processes of the olfactory, vomeronasal and terminalis nerves, which form the scaffold along which LHRH neurons migrate into the brain. Injection of a small amount (1 microliter) of antiserum to NCAM into the olfactory pits of 10-day-old embryonic mice, while not sufficient to break up the NCAM scaffolding, appeared to decrease the number of LHRH-immunoreactive cells in the epithelium of the medial olfactory pit, and retarded their migration in the nasal mesenchyme. This suggest that NCAM is important for LHRH cell migration. Never found actually colocalized with LHRH in the same neurons, NCAM nevertheless may be required for the migration of LHRH-expressing cells.

Adult↗
PubMed1988

Electrical stimulation of ascending noradrenergic tracts in the midbrain: suppression of steroid-induced luteinizing hormone release.

This study examined the effects of electrical stimulation of the dorsal and ventral ascending noradrenergic tracts in the central nervous system [dorsal (DNT) and ventral (VNT) noradrenergic tracts] during an ongoing LH surge induced by ovarian steroids. A bipolar electrode was implanted in the midbrain of ovariectomized rats, in the region of either the DNT or VNT. One week later the rats were given estradiol benzoate (10 micrograms/100 g BW), followed 3 days later by an injection of progesterone (2 mg) at 1100 h. This steroid treatment resulted in a LH surge in the afternoon which peaked at approximately 1800 h. Biphasic electrical stimulation (50-100 microA; 400 musec; 30 Hz) was applied to the conscious unrestrained rats for 1 h beginning at 1600 h. Electrical stimulation of the DNA (n = 10) for 1 h resulted in significantly lower LH levels at 1700 h. Similar electrical stimulation of the VNT (n = 8) also markedly suppressed LH release at 1700 h. Electrical stimulation of brain sites close to but outside the DNT or VNT were ineffective. After the cessation of electrical stimulation, LH levels began to rise again and at 1900 h were not significantly different from levels in the control rats. To determine if the recovering LH surge could be interrupted further, the effects of a second electrical stimulating session, 2 h after the first one, was investigated in other groups of animals. As expected, electrical stimulation of either the DNT or VNT between 1600 and 1700 h resulted in a transient suppression of the steroid-induced LH surge. The mean LH levels of these animals were on the rise between 1700 and 1900 h. Dramatically, a second electrical stimulation applied to the DNT or VNT from 1900-2000 h again inhibited LH release. Thus, the LH release pattern in these twice-stimulated rats was significantly different from that in either the nonstimulated controls or animals that had received only one electrical stimulation session (at 1600 h). Treatment of the rats with an alpha-adrenergic blocker (phenoxybenzamine) reversed the inhibitory effect of DNT activation on the LH surge. Treatment with a beta-adrenergic blocker (propranolol) or a dopamine antagonist (pimozide) was ineffective. These data demonstrate that, similar to intraventricular infusion of norepinephrine, activation of the ascending norepinephrine fibers results in interruption of the steroid-induced LH surge.

Animals↗
PubMed1987

Electrical stimulation of ventral versus dorsal mesencephalic tegmental areas in the conscious rat: effects on luteinizing hormone release.

This study examined the effect of electrical stimulation of the ventral mesencephalic tegmentum versus the dorsal tegmentum region on blood LH levels in freely moving, ovariectomized (OVX) rats, as well as in OVX, estrogen-primed rats. In OVX rats, electrical stimulation (with parameters of 30 Hz, 0.4-msec biphasic pulses, 50-100 microA and 10 s on/off for 1 h) of the ventral tegmentum region with the aim of activating the ventral noradrenergic tract (VNT) failed to affect the pulsatile pattern of blood LH levels characteristic of OVX animals. In sharp contrast, electrical stimulation of the dorsal tegmentum region inside the ascending dorsal noradrenergic tract (DNT) markedly inhibited pulsatile LH release in OVX rats; the mean blood LH levels during the 1-hour stimulation period were significantly decreased when compared with prestimulation control values. Electrical stimulation in the same region near but outside the DNT was ineffective. In OVX rats primed with estradiol benzoate, electrical stimulation in the ventral or dorsal tegmentum region failed to alter the low, nonpulsatile blood levels of LH. The results in OVX rats suggest that selective activation of the ascending noradrenergic fibres of the DNT but not the VNT can inhibit pulsatile LH release in the awake, freely moving animal. These data further support the possible existence of an inhibitory noradrenergic system in the modulation of LH release.

Animals↗
PubMed1986

Norepinephrine inhibition of pulsatile LH release: receptor specificity.

Infusion of norepinephrine (NE) into the third ventricle of ovariectomized (OVX) adult rats inhibits pulsatile luteinizing hormone (LH) secretion. This study examines the effects of pretreatment with specific alpha- and beta-adrenergic blockers on the subsequent NE-induced suppression of LH release. Unanesthetized long-term OVX rats were injected ip or iv with phenoxybenzamine (alpha-adrenergic receptor blocker), propranolol (beta-adrenergic blocker), or an equal volume of saline (as controls). Approximately 1-1.5 h later, the animals were given an intraventricular (ivt) administration of NE. Infusion of acidified saline into the third ventricle of OVX rats failed to affect the pulsatile pattern of LH release characteristic of these animals. After ivt of NE, the control rats showed a significant decrease in mean blood LH level of ca. 30%. Pretreatment of OVX rat with propranolol either ivt or ip failed to affect pulsatile LH release. Subsequent ivt infusion of NE either at 1 h or 15 min after propranolol treatment also caused a 28-30% decrease in the mean LH levels and suppressed pulsatile discharge of LH, an effect that lasted for approximately 45-50 min. In sharp contrast to the saline and propranolol-treated groups, rats pretreated with phenoxybenzamine had sporadic or no LH pulses during the 70-min postphenoxybenzamine period and had significantly lower mean LH levels when compared with control animals (P less than 0.05). Moreover, a drop in mean blood LH levels after NE infusion was not observed in the rats pretreated with phenoxybenzamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Suppression of progesterone-induced gonadotropin surge by adrenergic agonists in estrogen-primed ovariectomized rats.

An involvement of catecholamines in the preovulatory gonadotropin surge has been proposed for many years. Specifically, an alpha-adrenergic mechanism has been implicated in the stimulation of ovulation and LH release. On the other hand, little is known regarding the possible role of adrenergic neurotransmission once a gonadotropin surge has been initiated. In this study, drugs which affect adrenergic receptors were administered centrally to estrogen-primed ovariectomized rats and the effects on serum concentrations of LH and FSH induced by treatment with progesterone at 08:00 h were examined. As expected, the progesterone treatment caused a significant (p less than 0.05) increase in blood LH and FSH levels by 14:00 and 15:00 h, respectively, when compared with those seen at 13:00 h. In control rats that received isotonic saline intraventricularly at 15:00-16:00 h, both LH and FSH levels continued to rise linearly and reached peak levels by 17:00 and 18:00 h. By contrast, intraventricular infusion of norepinephrine at 16:00 h caused a significant decrease (p less than 0.05) in LH levels when compared with the saline-infused control groups. Moreover, rats that received intraventricular infusion of phenylephrine (an alpha 1-adrenergic agonist) at 15:00 h failed to show a significant increase in LH and FSH levels until 19:00 h; this inhibitory effect was mimicked by a relatively more specific alpha 1-adrenergic agonist, methoxamine. Consistent with our previous findings, animals which received intraventricular isoproterenol (a specific beta-adrenergic agonist) at 15:00 h also responded with suppressed serum LH levels at 16:00-19:00 h when compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1978

Surgical treatment of choledochal cyst.

A case of multiloculated choledochal cyst occurring in an 18-year-old girl is presented. The choledochus which contained multiple pigment stones was excised as the primary treatment and the patient remains well on two year follow-up. Ten additional cases of choledochal cyst treated in the past 20 years have been reviewed. It is concluded that excision of the choledochus is a safe and acceptable treatment of choledochal cyst in young low risk patients and that the alternative treatment of Roux-en-Y choledochocyst-jejunostomy gives satisfactory results.

Adolescent↗