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An unbiased place preference conditioning procedure was used to examine the role of delta-opioid receptors in mediating the aversive effects of opioid withdrawal. Rats were implanted s.c. with two pellets each containing placebo or 75 mg morphine. Single-trial conditioning sessions with saline and the opioid receptor antagonists naloxone (0.001-1.0 mg/kg, s.c.), naltrindole (0.01-3.0 mg/kg, s.c.) or naltriben (0.01-3.0 mg/kg, s.c.) commenced 4 days later. During these conditioning sessions, physical signs of withdrawal were also quantified. Tests of conditioning were conducted on day 5. Naloxone in doses of 0.01-1.0 mg/kg produced significant conditioned place aversions in morphine-implanted animals. A dose of 0.01 mg/kg produced few physical withdrawal signs whereas higher doses resulted in marked wet dog shakes, body weight loss ptosis and diarrhea. No such effects were observed in control (placebo-implanted) animals. Administration of the selective delta-opioid receptor antagonists naltrindole and naltriben produced dose-related place aversions in morphine-implanted animals. The magnitude of these effects did not differ from that observed with naloxone. The minimum effective doses of naltrindole and naltriben were 0.1 mg/kg. Doses of 0.1-1.0 mg/kg produced few, if any, somatic signs of withdrawal whereas higher doses of these antagonists only produced diarrhea and wet-dog shakes. Other withdrawal signs were absent. In contrast to the opioid receptor antagonists tested, the dopamine D1 receptor antagonist SCH23390 failed to produced conditioned place aversions or physical signs of withdrawal in morphine-pelleted animals. These data demonstrate that the selective blockade of either delta- or mu-opioid receptors is sufficient to induce conditioned aversive effects in morphine-dependent animals. They also indicate that physical symptoms associated with precipitated morphine withdrawal differ depending upon the opioid receptor antagonist employed.
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PMID:Role of delta-opioid receptors in mediating the aversive stimulus effects of morphine withdrawal in the rat. 874 Nov 60

A single dose toxicity of calcipotriol (MC903), an anti-psoriasic agent, administered subcutaneously (s.c.) and percutaneously (p.c.) was studied in Slc:SD rats (s.c. and p.c.) and beagle dogs (s.c.). The LD50 values of MC903 were as follows: rats, 2.19 mg/kg in males and 2.51 mg/kg in females by s.c., and more than 15 mg/kg in both sexes by p.c.; dogs, more than 1.5 mg/kg in males by p.c. No sexual difference was noted in LD50 values of rats. Death of rats was observed from 1 to 3 days after administration by both routes. Dead animals showed decreases in body weight and locomotor activity, reddish tear, abnormal gait and dirty hair by both routes. Furthermore, dead animals administered by s.c. showed salivation, nasal discharge, piloerection, ptosis, diarrhea, urorrhea, nasal and vaginal bleeding, subnormal temperature, loose stool, cyanosis, irregular and deep respirations, clonic and tonic convulsions. Survival of rats showed similar signs to those of dead animals except for nasal discharge, nasal and vaginal bleeding, cyanosis, agonal respiration and convulsion. Discoloration of the kidney, white patch of the heart and a dilatation of the stomach wall were observed on macroscopic examinations. No mortalities were observed in dogs which showed vomiting, conjunctival congestion, circumoral and auricular reddenings, periblepharal purplish reddening, decreases in locomotor activity and defecation, emaciation, eye discharge, skin desquamation of treated area and an increase in respiration. On macroscopic examination, desquamation of the skin, reddening of the circumoral mucosa, pale gray yellow striations in renal tubules of the cortex and discoloration of the thyroid were observed. Histopathological findings revealed epidermal thickening with parakeratosis, fibrocytes, hypertrophy and hypersecretion of the sebaceous and sweat glands, formation of epitheloid glanulomas and infiltration of neutrophils in the subcutaneous tissues. Furthermore, moderate calcium deposits in the renal tubules, fatty cells and slight calcium deposits in interstitial tissues of the thyroid, and a cystic nest of an ectopic intestinal epithelium between muscle layers of the duodenum were observed at the highest dose. On the basis of results obtained in the present study, rats administered MC903 by s.c. or p.c. died probably due to the circulatory and renal disturbance resulted from effects of this drug on the heart and kidney.
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PMID:[Single dose toxicity studies of calcipotriol (MC903) in rats and dogs]. 874 15

Abstinence from chronic morphine has been shown to reduce extracellular dopamine in the nucleus accumbens as measured by brain microdialysis (Acquas et al. 1991). In the present study, we investigated if similar changes take place in the prefrontal cortex. Withdrawal from a schedule of increasing doses of morphine administered intraperitoneally twice a day for 9 days up to a daily dose of 60 mg/kg resulted in doubling of basal extracellular concentrations of dopamine in the prefrontal cortex and in a mild withdrawal syndrome (ptosis, piloerection, hunched-back posture). Administration of a low dose of naloxone (0.5 mg/kg SC) to rats withdrawn from chronic morphine resulted in a full withdrawal syndrome with wet dog shakes and diarrhoea and an increase of extracellular dopamine that peaked at 40 min and returned to the pre-naloxone values by 80 min. The results show that dopamine neurotransmission in the medial prefrontal cortex responds to opiate withdrawal in a manner opposite to dopamine transmission in the nucleus accumbens and indicate that the dopamine system is affected by abstinence in a topographically specific manner, consistent with a different functional role of mesocortical as compared to mesolimbic dopamine systems.
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PMID:Increase of extracellular dopamine in the medial prefrontal cortex during spontaneous and naloxone-precipitated opiate abstinence. 884 38

Anorectal disorders are commonly encountered in the practice of emergency medicine. Most can be diagnosed and treated in the emergency department setting. Almost all anorectal disorders once diagnosed and treated in the emergency department need appropriate follow-up to ensure adequacy of treatment, for further possible diagnostic procedures (e.g., endoscopy, biopsy), or for definitive treatment. Hemorrhoids are the most prevalent anorectal disorder and are the most common cause of hematochezia. Treatment is dependent on the degree of hemorrhoid prolapse and symptoms. Most cases can be treated by conservative medical treatment (e.g., dietary changes, sitz baths) or nonsurgical procedures (e.g., rubber band liagation, infrared coagulation). Surgical excision of symptomatic thrombosed external hemorrhoids is indicated if within 48 to 72 hours of pain onset. Anal fissures are one of the most common causes of anorectal pain. They are most frequently idiopathic, and most are located in the posterior midline of the anal canal. Most anal fissures are adequately treated by a medical approach using sitz baths, stool softeners, and analgesics. If the anal fissure becomes chronic and is not responsive to medical therapy, a lateral sphincterotomy of the internal anal sphincter is the surgical procedure of choice. Pharmacologic treatment (botulinum toxin or nitroglycerin ointment) to decrease internal anal sphincter tone has shown promise in the treatment of anal fissure. Anorectal abscesses are categorized into four types: perianal, ischiorectal, intersphincteric, and supralevator. Most are idiopathic and contain mixed aerobic-anaerobic pathogens. Fistula formation varies from 25% to 50% and is much more common with gut-derived organisms (e.g., E. coli, B. fragilis). Definitive treatment for an anorectal abscess is timely surgical incision and drainage to prevent more serious complications (e.g., serious infection, extension of the abscess). Anal carcinomas are infrequent, the majority of them being squamous cell or epidermoid carcinomas. The emergency physician must maintain a high index of suspicion and obtain a biopsy of suspicious lesions in order not to miss the diagnosis of a cancer. The most common presenting complaint of anal tumors is rectal bleeding. Combination chemotherapy and radiotherapy have shown promising results in the treatment of anal canal tumors. Bacterial, viral, and protozoal infections can be transmitted to the anorectum via anoreceptive intercourse. Such infections must be considered when a patient presents with rectal pain or discharge, tenesmus, or rectal or perineal ulcers. Proctosigmoidoscopy and rectal cultures may be necessary to determine the cause. Potential rectal complications of HIV infection include infectious diarrhea, acyclovir-resistant strains of HSV2, Kaposi's sarcoma, lymphoma, and squamous cell carcinoma. Rectal injuries may result from penetrating or blunt trauma, iatrogenic injuries, or foreign bodies. Rectal injury should be suspected when a patient presents with low abdominal, pelvic, or perineal pain or blood per rectum after sustaining trauma or undergoing an endoscopic or surgical procedure. Tetanus prophylaxis, intravenous antibiotics, and surgical intervention are indicated in all but superficial rectal tears.
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PMID:Anorectal disorders. 892 68

The present study has examined the glycine/N-methyl-D-aspartate (NMDA) receptor antagonist, R-(+)-3-amino-1-hydroxypyrrolid-2-one (R-(+)-HA-966) and the competitive NMDA receptor antagonist, cis-4-(phosphonomethyl)piperidine-2-carboxylic acid (CGS 19755) on the behavioural syndrome and increased hipppocampal acetylcholine efflux induced during morphine-withdrawal in the rat. Subcutaneous naltrexone (1 mg/kg) injection, 48 hr after implantation of a 75 mg morphine pellet, induced a robust withdrawal syndrome consisting of wet dog shakes, ejaculations, mouth movement, ptosis, irritability to touch and diarrhoea. Pretreatment with the alpha2-adrenoceptor agonist, clonidine (0.1-0.4 mg/kg), R-(+)-HA-966 (10-60 mg/kg) or CGS 19755 (5 or 10 mg/kg) significantly reduced the incidence of withdrawal behaviours. In addition, all three compounds significantly attenuated the increase in hippocampal acetylcholine efflux induced following naltrexone (1 mg/kg, s.c.) injection in morphine-dependent rats. These results provide further evidence demonstrating that NMDA receptor antagonists attenuate both the behavioural and neurochemical effects observed during morphine withdrawal in the rat.
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PMID:Competitive and glycine/NMDA receptor antagonists attenuate withdrawal-induced behaviours and increased hippocampal acetylcholine efflux in morphine-dependent rats. 914 62

Shigella dysenteriae type 1 causes the most severe form of bacillary dysentery. The spectrum of illness ranges from mild watery diarrhoea to severe bloody diarrhoea. Shigellosis is often associated with intestinal complications, including intestinal perforation, intestinal obstruction, toxic dilatation of the colon, and prolapse of the rectum; systemic complications include septicaemia, hyponatraemia, hypoglycaemia, seizure, encephalopathy, haemolytic-uraemic syndrome, and malnutrition. Arthritis and conjunctivitis are rare extra-intestinal complications of shigellosis. Annually, about 110,000 patients receive treatment in the Dhaka Hospital of the International Centre for Diarrhoeal Disease Research, Bangladesh for diarrhoea and diarrhoea-associated illnesses, of which 11% are due to shigellosis. However, arthritis associated with shigellosis has not been reported from this population. Arthritis has been reported in association with infection due to S. flexneri and S. sonnei from other places. We are unaware of any reported case of arthritis in association with S. dysenteriae type 1 infections. In this report, we describe the clinical and laboratory features of a young woman who developed arthritis following S. dysenteriae type 1 infection.
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PMID:Reactive arthritis associated with Shigella dysenteriae type 1 infection. 930 97

Effects of agmatine, which is an endogenous polyamine metabolite formed by decarboxylation of L-arginine, were investigated on the morphine abstinence syndrome in rats. Two pellets containing 75 mg morphine base (total 150 mg) were implanted subcutaneously on the back of rats. Seventy-two hours after morphine implantation, agmatine sulphate (20, 30 and 40 mg/kg) or saline was injected intraperitoneally. Forty-five min later, naloxone (2 mg/kg) was injected intraperitoneally to induce precipitated withdrawal. Immediately after naloxone injection, rats were observed for 15 min, and abstinence syndrome signs, which included jumping, wet dog shake, writhing, defecation, ptosis, teeth chattering and diarrhea were counted or rated. Agmatine attenuated all of the signs of the morphine abstinence syndrome dose dependently and significantly. Our results suggest that agmatine prevents naloxone-precipitated abstinence syndrome in morphine dependent rats; thus, this drug may be beneficial in the treatment of opioid dependence.
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PMID:Inhibitory effect of agmatine on naloxone-precipitated abstinence syndrome in morphine dependent rats. 936 24

We report a 56-year old female with mitochondrial neurogastrointestinal encephalomyopathy (MNGIE), presenting with protein-losing gastroenteropathy and serum copper deficiency. There was no neuromuscular disease in her family members. Three years prior to admission, she developed severe gastrointestinal symptoms including diarrhea, nausea, vomiting and ascites, and was diagnosed as having protein-losing gastroenteropathy based on alpha(1)-antitrypsin clearance and other tests. She was referred to our department when neurological symptoms were apparent. Neurological examinations revealed bilateral ptosis, ophthalmoplegia, hearing loss, facial and limb muscle weakness, mild sensory deficit of vibration on her feet and hypoactive deep tendon reflexes. Pigmentary retinopathy, cerebellar ataxia and heart block were not seen. Serum copper level was decreased to 45 micrograms/dl (normal: 83-155). Chronic intestinal pseudo-obstruction was proven by X-ray studies, and diffuse leukoencephalopathy demonstrated on brain MRI. On EMG, motor nerve conduction velocities were prolonged with temporal dispersion. Her muscle biopsy from biceps brachii muscle showed both neuropathic and myopathic changes, scattered ragged-red fibers and focal cytochrome c oxidase deficiency. Southern blot and polymerase chain reaction analysis on mitochondrial DNA showed no deletions nor point mutations. The clinical and pathologic findings of the present patient fulfilled the diagnostic criteria of mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) proposed by Hirano et al. There are few reported patients with MNGIE in Japan, but none presented with protein-losing gastroenteropathy and serum copper deficiency. Since the copper is a cofactor of cytochrome c oxidase, decreased serum copper level may aggravate the respiratory chain enzyme metabolism in mitochondria. Therefore, treatment for gastrointestinal tract disturbance and copper administration may be necessary to prevent disease progression.
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PMID:[Mitochondrial neurogastrointestinal encephalomyopathy presenting with protein-losing gastroenteropathy and serum copper deficiency: a case report]. 949 Sep 4

The ability of a pretreatment with the cholecystokininB-receptor (CCK[B]) antagonist L-365,260 to prevent the development of morphine dependence was studied in normal and neuropathic (unilateral peripheral neuropathy) rats. A 4-day pretreatment regimen with two daily s.c. injections of either saline+saline, saline+morphine (3.0 mg/kg) or L-365,260 (0.2 mg/kg)+morphine was used, and withdrawal was precipitated by an injection of naloxone (1.0 or 2.0 mg/kg i.v.) at 24 h after the last pretreatment injection. After pretreatment with morphine alone, physical dependence developed in both normal and neuropathic rats. However, the incidence of teeth chattering and ptosis was higher in neuropathic rats. Pretreatment with the combination of L-365,260 and morphine prevented the expression of teeth chattering, ptosis, diarrhea, writhing and piloerection, but was devoid of effects on the exploratory activity among both groups of rats. These results suggest that endogenous CCK acting on CCK(B)-receptors may be involved in the development of morphine dependence both in normal and neuropathic rats.
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PMID:The selective cholecystokininB receptor antagonist L-365,260 diminishes the expression of naloxone-induced morphine withdrawal symptoms in normal and neuropathic rats. 949 17

Effects of gamma-vinyl-GABA (GVG), an antiepileptic drug that inhibits GABA transaminase and increases extracellular GABA concentrations in the brain, were investigated on the morphine abstinence syndrome (AS) in male Wistar rats. Two morphine pellets (75 mg morphine base in each) were implanted subcutaneously on the back of the rats. Seventy-two hours after the morphine implantation, naloxone (NL, 2 mg kg-1) was injected intraperitoneally (i.p.) to induce precipitated morphine AS. GVG was administered at the doses of 250 mg kg-1 (n = 11) and 500 mg kg-1 (n = 11) i.p. 24 h prior to AS and at the dose of 500 mg kg-1 (n = 13) i.p. 6 h prior to AS. Immediately after NL injections, rats were observed for 5 min and AS signs (jumping, teeth chattering, wet dog shake, diarrhoea, ptosis and defecation) were assessed. The behavioural signs of GVG-treated rats were compared with the control groups (n = 10) during the AS. Jumping, wet dog shake, teeth chattering were found to be significantly increased in all of the GVG-treated groups. Ptosis was found to have increased in only 500 mg kg-1 GVG groups. GVG potentiated the severity of morphine AS signs. GVG does not seem to have any therapeutic potential for treatment of morphine abstinence unlike some other drugs that enhance GABAergic transmission.
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PMID:Gamma-vinyl-GABA potentiates the severity of naloxone-precipitated abstinence signs in morphine-dependent rats. 969 54


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