Exercise training, creatine supplementation, and bone health in ovariectomized rats.

UNLABELLED: Evidence suggests that creatine may have some beneficial effects on bone. The study aimed to investigate the effects of exercise alone or combined with creatine on bone health in ovariectomized rats. Findings show that exercise, but not creatine, has an important role in improving bone health. INTRODUCTION: The aim of this study was to investigate the effects of exercise training alone or combined with creatine supplementation on bone health parameters in ovariectomized rats. METHODS: Wistar rats were randomly allocated into one of five groups: (i) sham-operated, (ii) ovariectomized non-trained placebo-supplemented, (iii) ovariectomized non-trained creatine-supplemented, (iv) ovariectomized exercise-trained placebo-supplemented, and (v) ovariectomized exercise-trained creatine-supplemented. Downhill running training and/or creatine supplementation (300 mg/kg body weight) were administered for 12 weeks. Bone mineral content (BMC), bone mineral density (BMD), and biomechanical and histomorphometric parameters were assessed. RESULTS: No interaction effects were observed for BMC and BMD at whole body, femur, and lumbar spine (p > 0.05). Importantly, a main effect of training was detected for whole body BMC and BMD (p = 0.003 and p < 0.001, respectively), femoral BMC and BMD (p = 0.005 and p < 0.001, respectively), and lumbar spine BMC and BMD (p < 0.001 and p < 0.001, respectively), suggesting that the trained animals had higher bone mass, irrespective of creatine supplementation. Main effects of training were also observed for maximal load (p < 0.001), stiffness (p < 0.001), and toughness (p = 0.046), indicating beneficial effects of exercise training on bone strength. Neither a main effect of supplementation nor an interaction effect was detected for biomechanical parameters (p > 0.05). No main or interaction effects were observed for any of the histomorphometric parameters evaluated (p > 0.05). CONCLUSIONS: Exercise training, but not creatine supplementation, attenuated ovariectomy-induced bone loss in this rat model.

A Comparative Study of Hummingbirds and Chickens Provides Mechanistic Insight on the Histidine Containing Dipeptide Role in Skeletal Muscle Metabolism.

Histidine containing dipeptides (HCDs) have numerous ergogenic and therapeutic properties, but their primary role in skeletal muscle remains unclear. Potential functions include pH regulation, protection against reactive oxygen/nitrogen species, or Ca2+ regulation. In recognition of the challenge of isolating physiological processes in-vivo, we employed a comparative physiology approach to investigate the primary mechanism of HCD action in skeletal muscle. We selected two avian species (i.e., hummingbirds and chickens), who represented the extremes of the physiological processes in which HCDs are likely to function. Our findings indicate that HCDs are non-essential to the development of highly oxidative and contractile muscle, given their very low content in hummingbird skeletal tissue. In contrast, their abundance in the glycolytic chicken muscle, indicate that they are important in anaerobic bioenergetics as pH regulators. This evidence provides new insights on the HCD role in skeletal muscle, which could inform widespread interventions, from health to elite performance.

Acute stimulation of prolactin release by estradiol: mediation by the posterior pituitary.

We have previously shown that the posterior pituitary contains a potent PRL-releasing factor (PRF). Estradiol stimulates PRL release by acting at three possible sites: the hypothalamus, the anterior pituitary, and the posterior pituitary. The objectives were 1) to document the profiles of PRL and LH release in response to an acute administration of estradiol, and 2) to identify the site of action of estradiol by employing two surgical approaches, pituitary stalk section (SS) and posterior pituitary lobectomy (LOBEX). Ovariectomized rats were used throughout. In Exp 1, rats were injected iv with 5 micrograms/kg 17 beta-estradiol, and blood was collected at 30-min intervals for 4 h. Estradiol induced a rapid and profound decline in plasma LH levels and a delayed, 5- to 6-fold rise in PRL. The purpose of the second experiment was to determine whether estradiol stimulates PRL release by acting at the anterior pituitary. Injection of estradiol to SS rats failed to stimulate a rise in PRL. We have previously reported that lactotrophs of SS rats are responsive to PRL secretagogues such as TRH. The objective of the third experiment was to differentiate between hypothalamic and posterior pituitary sites of estradiol action. Estradiol induced only a small rise in PRL when injected into LOBEX rats. However, LOBEX and control rats showed similar large rises in PRL in response to injection of alpha-methyl-para-tyrosine, an inhibitor of tyrosine hydroxylase. The latter indicates that the hypothalamic dopaminergic system as well as anterior pituitary lactotrophs are functionally intact in LOBEX rats. We conclude that estradiol administration to ovariectomized rats induces a rapid decline in LH and a delayed marked increase in PRL. The posterior pituitary, probably via PRF, is the primary site that mediates the acute effects of estradiol on PRL release. Estradiol does not stimulate PRL release directly from the anterior pituitary. The role of the hypothalamus is unclear. Estradiol could act directly on PRF-containing cells in the posterior pituitary or indirectly, via hypothalamic neurons terminating in the posterior pituitary. The hypothalamus also has a minor component that responds to estradiol and is independent of the posterior pituitary.

Posterior pituitary lobectomy abolishes the suckling-induced rise in prolactin (PRL): evidence for a PRL-releasing factor in the posterior pituitary.

UNLABELLED: The aim of this study was to determine the role of the posterior pituitary in the regulation of PRL release during suckling. Lactating rats were subjected to posterior pituitary lobectomy (LOBEX) or sham surgery (SHAM) and separation from pups in the evening; experimental manipulations and blood collection were performed the next morning. In the first experiment rats were divided into three groups: SHAM, LOBEX, and LOBEX treated with a vasopressin analog, 1-desamino-8-D-arginine vasopressin and oxytocin. Plasma PRL levels in SHAM rats increased 20- to 25-fold upon introduction of pups and remained elevated for the duration of suckling. In contrast, basal plasma PRL levels in LOBEX rats were 3- to 4-fold higher than in SHAM but suckling failed to induce a further increase. Treatment of LOBEX rats with 1-desamino-8-D-arginine vasopressin and oxytocin reduced water consumption and allowed for milk ejection and milk intake by the pups but did not restore the suckling-induced rise in PRL. The second experiment tested the functional integrity of the hypothalamic dopamine (DA) and serotonergic systems after LOBEX and the ability of LOBEX-lactating rats to respond to PRL-releasing stimuli other than suckling. Injections of alpha-methyl-para tyrosine, an inhibitor of tyrosine hydroxylase, and 5-hydroxytryptophan, a precursor of serotonin, caused 20- to 30-fold rises in plasma PRL levels in both LOBEX and SHAM rats. Exposure to ether elicited a 3- to 4-fold rise in PRL which was higher in magnitude and of longer duration in LOBEX than in SHAM rats. CONCLUSIONS: Removal of the posterior pituitary from lactating rats results in an increase in basal PRL levels and a complete abolishment of the suckling-induced rise. Vasopressin and oxytocin restore water balance and milk ejection in the LOBEX rat but fail to affect PRL secretion. The LOBEX-lactating rat is not refractory to PRL-releasing stimuli other than suckling and its hypothalamic DA and serotonergic systems are functionally intact. In addition to DA, the posterior pituitary appears to contain a PRL-releasing factor(s) which mediates the suckling-induced rise in PRL.

The peak phase of the proestrous prolactin surge is blocked by either posterior pituitary lobectomy or antisera to vasoactive intestinal peptide.

UNLABELLED: The proestrous surge of PRL could result from a decrease in dopamine, an increase in PRL-releasing factor (PRF) or both. The objectives were to determine whether PRF from the posterior pituitary regulates the proestrous PRL surge, and to examine if there are interactions between PRF and vasoactive intestinal peptide (VIP). Posterior pituitary lobectomy (LOBEX) and passive immunization against VIP were employed. Adult cycling rats were subjected at 0900 h on proestrus to LOBEX or sham surgery (SHAM) under short term anesthesia, and were injected iv at 1330 h with 0.75 ml anti-VIP serum or normal rabbit serum. Jugular blood was collected hourly from 1400-2300 h and analyzed for PRL and LH by RIA. Oviductal ova were examined on estrus. The rise in plasma PRL in normal rabbit serum-treated SHAM rats was biphasic, with an early peak between 1500-1700 h and a lower plateau between 1900-2100 h. This rise was similar in profile and magnitude to that seen in intact rats. In contrast, LOBEX significantly attenuated the early peak, but did not alter the plateau. Passive immunization against VIP of either SHAM or LOBEX rats mimicked the effect of LOBEX alone on PRL release. Neither surgery nor anti-VIP serum affected the profile of the LH surge which was sharp and symmetrical, and all rats ovulated with 15-16 ova per rat. To determine whether VIP is the posterior pituitary PRF, selected tissues removed on proestrus or diestrus-1 were analyzed for VIP by RIA. VIP was undetectable (less than 20 pg/organ) in the posterior pituitary on either day examined. The contents of VIP in the anterior pituitary, medial basal hypothalamus, and paraventricular nuclei were unchanged between diestrus-1 and proestrus. CONCLUSIONS: The proestrous surge of PRL consists of two components: an early peak and a late plateau. The peak phase appears to be dependent on PRF input from the posterior pituitary. This input might be regulated by VIP, and interactions between the two could occur at the level of the hypothalamus, anterior pituitary, or both. The plateau phase of the PRL surge is independent of the posterior pituitary and VIP, and might involve hypothalamic dopamine.

Time-dependent increase in plasma prolactin after pituitary stalk section: role of posterior pituitary dopamine.

PRL secretion is inhibited by dopamine (DA) input from two systems: the tuberoinfundibular (TIDA) with terminals in the median eminence, and the tuberohypophyseal (THDA) with terminals in the posterior pituitary. The aims of this study were 1) to determine the effects of pituitary stalk section (SS), which prevents DA input from the TIDA neurons, on PRL release, and 2) to assess if the anterior pituitary receives any DA input after SS. Ovariectomized rats were subjected to SS or sham surgery. Jugular blood was collected on the day of surgery (day 0) and for 6 days thereafter and was analyzed for PRL by RIA. DA concentration in the posterior pituitary was determined by HPLC. Unexpectedly, SS caused only a 2- to 3-fold initial rise in plasma PRL on day 0. This was followed by a gradual rise to 4-, 6-, and 8-fold above control levels on days 2, 4, and 6, respectively, without a further increase by 2 weeks. During this time, DA concentrations in the posterior pituitary progressively declined to 66%, 28%, and 6% of control values on days 1, 2, and 6 after SS, respectively. In the second experiment, intact and SS rats were treated with the DA receptor antagonist haloperidol. Haloperidol induced a dramatic 30- to 40-fold increase in plasma PRL in intact rats. Haloperidol induced a 3-fold rise in plasma PRL on day 1 after SS and a transient 2.5-fold rise on day 2. On day 6 after SS, when DA in the posterior pituitary was barely detectable, haloperidol failed to increase PRL secretion. The DA agonist apomorphine caused similar inhibitions of PRL release on days 1 and 6 after SS. Injections of TRH stimulated PRL secretion equally well in intact and SS rats. We conclude that SS does not induce refractoriness to PRL secretagogues or a dysfunction of the anterior pituitary DA receptors. The immediate rise in PRL after SS is modest because the anterior pituitary still receives DA input from the posterior pituitary. A gradual exhaustion of posterior pituitary DA, caused by the disconnection of the THDA terminals from their perikarya, leads to the progressive rise in plasma PRL levels. The DA input affecting PRL release is derived exclusively from the TIDA and THDA neurons, but their relative contributions are yet unknown.

The rat posterior pituitary contains a potent prolactin-releasing factor: studies with perifused anterior pituitary cells.

UNLABELLED: We previously reported that removal of the posterior pituitary abolished the suckling-induced rise in plasma PRL. This suggested that the posterior pituitary contains a PRL-releasing factor (PRF). Using perifused anterior pituitary cells, the objectives of this study were 1) to examine whether the posterior pituitary contains PRF activity as compared to the medial basal hypothalamus (MBH), and 2) to determine to what extent substances known to be present in the posterior pituitary and/or MBH contribute to this activity. Anterior pituitary cells, attached to Cytodex beads, were perifused with medium 199. Tissues were extracted with acid, lyophilized, and reconstituted in medium 199. Tissue extracts and synthetic compounds were introduced to the cells in short pulses. Fractions were collected and analyzed for PRL, LH, and GH by RIA. Posterior pituitary extracts contained a potent substance(s) which stimulated PRL release in a concentration-dependent manner, but did not alter LH secretion. As little as 1% of the extract increased PRL release. In contrast, the MBH extract contained significantly less PRF activity but was capable of stimulating and inhibiting LH and GH release, respectively. Cerebellar extracts did not alter PRL secretion. Of more than 25 neuroactive substances tested in the perifusion system, oxytocin, TRH, and angiotensin II (A II) appeared as likely candidates for PRF. Therefore, the specific receptor antagonists d(CH2)5Tyr(Me) ornithine vasotocin (for oxytocin), chlordiazepoxide (for TRH), or saralasin (for A II) were infused together with the posterior pituitary extract. These antagonists completely abolished the PRL-releasing activities of their respective peptides but failed to reduce the PRF activity of the posterior pituitary. In contrast, PRF activity in the MBH was nearly eliminated by the TRH antagonist. CONCLUSIONS: 1) The rat posterior pituitary contains a potent PRF capable of inducing a rapid, hormone-specific, concentration-dependent stimulation of PRL release from perifused anterior pituitary cells. 2) The MBH contains significantly less PRF activity, which is largely attributable to TRH. 3) Although the chemical identity of PRF is yet unknown, the PRF activity in the posterior pituitary is not accounted for by oxytocin, TRH, or A II.

Circadian rhythm of melatonin and prostaglandin in modulation of stress-induced gastric mucosal lesions in rats.

BACKGROUND: We previously demonstrated the circadian variation of water-immersion restraint stress (WRS)-induced gastric mucosal lesions in rats. AIM: To investigate the roles of melatonin and prostaglandin in the gastric mucosa in circadian modulation of WRS. METHODS: Fasted rats were subjected to 4-h WRS during both the diurnal and nocturnal phases of a light/dark cycle. Mucosal lesions, serum melatonin concentrations, mucosal generation of prostaglandin E2 (PGE2) and mucosal gene expressions of cyclooxygenase (COX)-1 and -2 were evaluated. RESULTS: Lesion area after 4-h stress during the dark phase was significantly smaller than that in light-phase controls. Serum melatonin concentration in control rats during the light phase was significantly increased 4 h after WRS, but PGE2 generation was decreased by 48% as compared to that in intact mucosa before stress. In the dark phase, melatonin concentration after 4-h WRS was significantly depressed as compared with the control level at the corresponding time. PGE2 concentrations after 4-h WRS in the dark phase were not decreased compared with the control level at the corresponding time, although PGE2 level was significantly lower than that in light-phase controls. Expression of COX-1 and COX-2 mRNA was detected after exposure to stress in both the light and dark phases. CONCLUSION: These results suggest that circadian rhythm has an important role in the formation of stress-induced gastric mucosal lesions in rats. The circadian rhythm of melatonin responses and PGE2 generation may contribute to nocturnal/diurnal rhythmicity of gastric mucosal defences between day and night.

Central effect of melatonin against stress-induced gastric ulcers in rats.

We investigated the role of melatonin in the induction of gastric lesions induced by water immersion restraint stress or centrally administered thyrotropin-releasing hormone (TRH). Melatonin (0.1-1 ng) injected intracisternally (i.c) 30 min prior to stress dose-dependently inhibited the induction of gastric lesions by water immersion restraint stress, while 100 micrograms/kg, i.p. failed to protect the gastric mucosa. Preadministration of melatonin (1 ng, i.c.) significantly reduced (83%) the severity of gastric lesions induced by a TRH analogue (500 ng, i.c.). Serum melatonin concentrations 30 min after administration of 1 ng melatonin i.c. did not differ from those of rats receiving i.c. vehicle. These results suggest that melatonin plays a protective, anti-stress, role in the gastric mucosa via a mechanism involving the central nervous system.

Central nervous system action of melatonin on gastric acid and pepsin secretion in pylorus-ligated rats.

We recently demonstrated that centrally administered melatonin at low doses inhibits the induction of gastric lesions by water-immersion restraint stress. To investigate the mechanism of the potent anti-ulcer action of melatonin, the central nervous system (CNS) effects of melatonin on gastric acid and pepsin secretion were studied in conscious pylorus-ligated rats. Intracisternal (i.c.) melatonin (1-100 ng) dose-dependently decreased acid and pepsin output, while a higher i.p. dose (1 microg) had no inhibitory effect. The i.c. melatonin did not change serum gastrin concentrations. Serum melatonin concentrations at 1 and 4 h after i.c. administration of 10-100 ng melatonin did not differ from those in rats receiving i.c. vehicle. The present results suggest that melatonin administered centrally modulates the secretion of gastric acid and pepsin which may explain, at least in part, the protective, anti-stress role of melatonin in the gastric mucosa observed in our previous study.

Central nervous system action of melatonin on gastric acid and pepsin secretion in pylorus-ligated rats.

We recently demonstrated that centrally administered melatonin at low doses inhibits the induction of gastric lesions by water-immersion restraint stress. To investigate the mechanism of the potent anti-ulcer action of melatonin, the central nervous system (CNS) effects of melatonin on gastric acid and pepsin secretion were studied in conscious pylorus-ligated rats. Intracisternal (i.c.) melatonin (1-100 ng) dose-dependently decreased acid and pepsin output, while a higher i.p. dose (1 microg) had no inhibitory effect. The i.c. melatonin did not change serum gastrin concentrations. Serum melatonin concentrations at 1 and 4 h after i.c. administration of 10-100 ng melatonin did not differ from those in rats receiving i.c. vehicle. The present results suggest that melatonin administered centrally modulates the secretion of gastric acid and pepsin which may explain, at least in part, the protective, anti-stress role of melatonin in the gastric mucosa observed in our previous study.

Prolactin secretion in posterior pituitary lobectomized rats: differential effects of 5-hydroxytryptophan and ether.

The objective of this study was to determine whether the posterior pituitary mediates the prolactin (PRL) releasing activities of serotonin and ether. Ovariectomized (OVEX) rats were subjected to posterior pituitary lobectomy (LOBEX) or sham surgery (SHAM). Either 1 or 12 days after surgery, rats were injected i.v. with 20 mg/kg b. wt. of 5-hydroxytryptophan (5-HTP), which is a precursor of serotonin. A second group of rats was exposed to ether vapors for 10 min. Blood was collected from a jugular cannula before and after the treatments and analyzed for PRL. On either 1 or 12 days after surgery, injection of 5-HTP increased plasma PRL levels 5-10 fold in both LOBEX and SHAM rats. This was followed by a decline to preinjection levels within 60-90 min. LOBEX and SHAM male rats which were injected i.p. with 50 mg/kg b. wt. of 5-HTP, also showed marked and similar elevations of plasma PRL levels 12 days after surgery. Exposure of OVEX rats to ether elicited a 2-3 fold rise in plasma PRL levels only on day 1, but not on day 12, after LOBEX. The ether-induced rise in PRL was similar in SHAM rats tested on both days. These results indicate that the 5-HTP-induced rise in plasma PRL levels is independent of the posterior pituitary, regardless of the sex, the route of drug administration or the length of time after surgery. In contrast, the PRL response to ether stress is diminished within 12 days after LOBEX. The evidence that the PRL responses to 5-HTP and to ether might be mediated via different neuronal mechanisms is discussed.

The pineal gland is not essential for circadian expression of rat period homologue (rper2) mRNA in the suprachiasmatic nucleus and peripheral tissues.

To investigate the functional involvement of the pineal gland in circadian expression of the rat period homolog gene (rPer2) in the suprachiasmatic nucleus (SCN) and peripheral tissues, we performed Northern blot analysis in tissues from pinealectomized rats. The ectomy did not have any significant effects on rPer2 mRNA expression patterns both in a daily light-dark condition and in a constant darkness. These results suggest that the rhythmic secretion of pineal melatonin is not essential for the circadian expression of clock genes in the SCN and other peripheral tissues of rats.

Detection of varicella-zoster virus DNA by polymerase chain reaction in cerebrospinal fluid of patients with herpes zoster meningitis.

In three of five patients with herpes zoster meningitis, varicella-zoster virus (VZV) DNA was detected by the polymerase chain reaction (PCR) in the initial samples of cerebrospinal fluid. DNA fragments of group A or B, following classification of VZV strains by the size of the variable region IV of VZV genome, were found at the 7th, 10th and 24th illness day in the three positive cases: one of these cases did not have skin lesions. These results suggest that the detection of VZV DNA by PCR is useful for the diagnosis of herpes zoster meningitis, as well as for its molecular epidemiology.

Melatonin's gastroprotective and antistress roles involve both central and peripheral effects.

Systemic administration of melatonin (5 to 20 mg/kg) has been reported to inhibit the induction of acute gastric mucosal lesions by stress or ischemia-reperfusion in rats. We recently demonstrated that intracisternal (i.c.) melatonin at low doses (1 to 100 ng) dose-dependently decreased acid and pepsin outputs in rats. The aim of the present study was to further investigate the peripheral and central roles of melatonin in gastric mucosal defense. Using a radioimmunoassay, we measured melatonin concentrations in the plasma and cerebrospinal fluid (CSF) of the cisterna magna in rats subjected to water immersion restraint stress and given intraperitoneal (i.p.) or i.c. injection of melatonin. Water immersion restraint stress was followed by a significant duration-related increase in peripheral plasma melatonin levels; the stress similarly produced a time-dependent increase in the extent of gastric mucosal lesions. Administration of melatonin (1 or 10 mg/kg, i.p., or 100 ng/10 microl, i.c.) significantly reduced the extent of stress-induced gastric damage, by 46%, 67%, and 54%, respectively. The effective i.c. dose of melatonin was at least 10,000-fold smaller than the effective i.p. dose. Melatonin levels in plasma and CSF after the i.p. injection of melatonin at 10 mg/kg were dramatically higher than those after the i.c. injection of vehicle or 100 ng of melatonin. Our results suggest that the peripheral gastroprotective action of melatonin should be investigated with due regard to these central effects.

Pathologic mechanism of experimental scoliosis in pinealectomized chickens.

STUDY DESIGN: This study was designed to investigate the pathologic mechanisms of idiopathic scoliosis using experimentally induced scoliosis in chickens. OBJECTIVE: To understand the process of producing a scoliotic deformity in pinealectomized chickens. SUMMARY OF BACKGROUND DATA: Pinealectomy in chickens consistently produces scoliosis with anatomic characteristics similar to those of human idiopathic scoliosis. Pinealectomized chickens are an important animal model for the study of idiopathic scoliosis. METHODS: In this study, 40 chickens were divided into two groups; 20 chickens treated with pinealectomy and 20 with a sham operation as control subjects on the second after hatching. The chickens in both groups then were killed at intervals ranging from 1 to 20 weeks after surgery. Their spines were examined visually and radiologically for the presence of a scoliotic curve and vertebral deformities. RESULTS: Rotational lordoscoliosis developed in pinealectomized chickens. The chickens with severe scoliosis were characterized by apically wedge-shaped vertebrae. In contrast, no scoliosis with any vertebral deformity developed in any of the chickens that received a sham operation. CONCLUSIONS: Because there normally is evidence of lordosis in the thoracic spine of chickens, the rotational instability of the spine induced by pinealectomy may produce a scoliotic deformity as a secondary phenomenon. Pinealectomy in chickens consistently produces scoliosis with anatomic characteristics similar to those of human idiopathic scoliosis. The authors believe that disturbance of the equilibrium and the posture mechanism associated with a defect in melatonin synthesis after pinealectomy may promote the development of rotational lordoscoliosis.

Role of serotonin for scoliotic deformity in pinealectomized chicken.

STUDY DESIGN: The effect of intraperitoneal injection of 5-hydroxytryptophan (5-HTP) versus control in pinealectomized chickens. OBJECTIVE: To find if the serotonin may have some role in the cause of treatment of idiopathic scoliosis. SUMMARY OF BACKGROUND DATA: One of the causes of idiopathic scoliosis is thought to be the disruption of postural reflex. Serotonin has been proposed to have a crucial role in maintaining normal postural muscle tone or postural equilibrium. METHOD: Forty pinealectomized chickens served as controls, and an additional 40 pinealectomized chickens received daily intraperitoneal injections of 5-hydroxy-tryptophan, a precursor of serotonin, which can pass through the blood-brain barrier. Spine radiographs were examined to measure the scoliotic deformity. RESULTS: Scoliosis developed in all 40 pinealectomized chickens (control), whereas only 28 chickens in the 5-hydroxytryptophan-treated group (6 in severe, 22 in mild) had scoliosis developed. The remaining 12 chickens grew up with normal spines. Most chickens with mild scoliosis did not have curve progression but continued to have wedged vertebrae. CONCLUSION: Serotonin deficit secondary to a defect of melatonin may have disturbed postural muscle tone or postural equilibrium resulting in scoliosis in pinealectomized chicken. Prevention from the development of scoliosis or its progression in chickens treated with 5-hydroxytryptophan suggests that serotonin may have potential therapeutic value.

Pathogenesis of idiopathic scoliosis. Experimental study in rats.

STUDY DESIGN: A radiographic examination of pinealectomized rats to observe the development of scoliosis and halt the condition by administration of melatonin. OBJECTIVES: To discover whether pinealectomy has the same effect in mammals as shown in the chicken, and to determine whether the bipedal condition is important for development of scoliosis. SUMMARY OF BACKGROUND DATA: Pinealectomizing chickens shortly after hatching consistently resulted in scoliosis closely resembling human idiopathic scoliosis. It has not been determined whether this phenomenon is restricted solely to chickens, or if this experimental model is applicable to other animals, especially those more closely related to humans. METHODS: A sham operation in five bipedal rats served as the control in this study. Pinealectomy was performed in 10 quadrupedal rats, pinealectomy in 20 bipedal rats, and pinealectomy with implantation of melatonin pellet in 10 bipedal rats. Spinal radiographs were used to measure the degree of scoliosis at 3 months after surgery. RESULTS: Scoliosis developed only in pinealectomized bipedal rats and not in quadrupedal rats. It developed in none of the sham operation group and in only 1 of 10 pinealectomized bipedal rats with melatonin treatment. CONCLUSIONS: Melatonin deficiency secondary to pinealectomy alone does not produce scoliosis if the quadrupedal condition is maintained. The bipedal condition, such as that in chickens or humans, plays an important role in the development of scoliosis. The findings suggest a critical influence of a postural mechanism for the development of scoliosis.

Measurement of radiation leaked from a 45-MeV linear accelerator facility by gated counting.

By the gated counting method that had been developed by the authors the spatial dose distributions at the boundary and inside of a 45-MeV electron linear accelerator (linac) facility were obtained using a NaI(Tl) scintillation probe and a counting system. Both distributions of pulse height and radiation propagation time were also measured. At the facility boundary, dose rates measured ranged from 0.16 microR hr-1 to 0.86 microR hr-1, which were less than one-tenth the natural background. At measurement in the linac control room, two different leakage sources, one originating at and around the accelerator and the other at a microwave power system, were discriminated by measuring pulse height and time distributions simultaneously.

Use of a gated counting method for radiation monitoring at a 45-MeV electron LINAC facility.

A fixed-point radiation monitoring system based on the gated counting method, which was previously reported by us, was constructed for a 45-MeV electron LINAC facility. It was tested under different beam intensities of the accelerator both at the current and repetition rates. It showed excellent dynamic response (from 2.5 X 10(-11) to 1.0 X 10(-8) Sv h-1) to the intensity variation of the radiation source. It was demonstrated that the system was very useful in monitoring an extremely low-level radiation from a pulsed source.