Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dysthyroid optic neuropathy (DON) was diagnosed in 36 eyes of 21 patients with progressive visual loss and congestive ophthalmopathy. Systemic features in the patients with DON did not differ from those reported for Graves' disease patients except that patients with DON were older (mean age, 61 years) and did not show female preponderance. Congestive symptoms always preceded visual loss, which was gradual in onset and bilateral in most patients but acute and asymmetrical in several. Presenting acuities were poorer than 20/60 in 50% of cases; central scotomas, sometimes combined with inferior depression, were the predominant field defects. Congestive signs were of moderate intensity without severe proptosis or exposure keratopathy. Bilateral and symmetrical ductional restriction was the most common motility disturbance. Oral corticosteroids were effective in restoring visual function in ten of 21 eyes treated. Many steroid-unresponsive eyes were improved promptly by supervoltage orbital irradiation or surgical decompression. In general, therapeutic intervention appeared to hasten recovery and improve visual outcome.
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PMID:Dysthyroid optic neuropathy. Clinical profile and rationale for management. 66 28

This paper presents the case of a 29 year-old male with a left ethmoidal pyocele with orbital and intracranial extensions causing proptosis and a temporal visual field defect of the left eye. The patient had a history of nasal injury as a result of traffic accident eleven years ago, and was well until four months prior to his first visit at which time he had an onset of left eye pain, proptosis, and blurring of vision developed following a URI episode. Since then, fluctuation of symptoms was noted with exacerbation when contracting a common cold. The left ethmoidal pyocele was diagnosed via clinical features and roentgenographic findings. The patient received a Caldwell Luc Operation with endonasal ethmoidectomy and the postoperative condition was good except for constriction of the entire visual field and the depression of temporal internal isopters of the left eye.
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PMID:[Proptosis and optic nerve compression caused by unilateral ethmoidal pyocele: a case report]. 165 46

The present study examined the behavioural effects of sigma agonists and PCP-like non-competitive N-methyl-D-aspartate (NMDA) antagonists in guinea-pigs. Subcutaneous (SC) injection of the putative sigma agonist (+)NANM (1 and 10 mg/kg SC) and (-)NANM (1 and 10 mg/kg SC) produced a behavioural response in guinea-pigs which was characterized by sedation and exophthalmos, with locomotor depression, flattened posture and flaccidity, whereas the sigma ligand pentazocine induced sedation but no flattened posture. Ketamine (20 mg/kg SC) and (+)dizocilpine (0.025, 0.1 and 1 mg/kg SC) produced similar effects to those of (+) and (-)NANM. However, the putative sigma receptor ligand DTG (1 and 10 mg/kg SC) had no observable effect on behaviours in guinea-pigs, similar to results for other species. The behavioural effects produced by (+) and (-)NANM were not reversed by injection 1 h later of naloxone hydrochloride (15 mg/kg SC), haloperidol (10 mg/kg SC) or DTG (10 and 30 mg/kg SC), but the effects of all drugs were reversed by the selective dopamine D-2 agonist quinpirole (3 mg/kg IP). Moreover, injection of naloxone (15 mg/kg SC), DTG (10 and 30 mg/kg SC) or haloperidol (1 and 10 mg/kg SC) 10 min before, did not reverse the behaviour induced by (+)NANM (10 mg/kg SC). These data indicate that sigma and PCP-like drugs have a similar gross behavioural effect in guinea-pigs, possibly mediated by non-competitive antagonism of the NMDA subtype of glutamate receptors. The results demonstrating behavioural depression were in contrast to the stimulatory effects of these drugs at similar doses in other rodent species.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Similar behavioural effects of sigma agonists and PCP-like non-competitive NMDA antagonists in guinea-pigs. 168 18

Methylenedioxymethamphetamine (MDMA) was administered to dogs and rats orally once a day for a 28-day period to evaluate the morphological and neuropathological effects. Major clinical signs associated with the administration of MDMA in the dog included circling, depression, dilated pupils, hyperactivity, rapid breathing, and salivation. Major clinical signs in the rat included hyperactivity, excitability, piloerection, exophthalmos, and salivation. Gross observations at necropsy in the dog possibly related to administration of the test article included reduced testicular size (one high and one medium dose) and prostatic enlargement in two high-dose animals. No gross lesions were seen in the rats at necropsy. The medium- and the high-dose groups in both sexes in both the rats and the dogs gained significantly less weight than the control and low-dose groups. Food consumption decreased the first week for the high- and medium-dose groups, but a significant reversal toward more normal consumption was noted in the following weeks in both the rats and the dogs. Hematologic, clinical chemistry, and urinalysis values did not appear to be affected by the administration of the test article in the dog. In the rat clinical pathology variables showing a trend to decrease with dose included urinary pH, blood urea nitrogen, glucose, creatinine (females), lactate dehydrogenase (LDH) (females), and chloride. Clinical pathology variables showing a trend to increase with dose included total white blood cell count and phosphorus. Microscopically, testicular atrophy was present in one medium-dose and two high-dose male dogs. Prostatic hyperplasia was present in two high-dose male dogs. No test article-related lesions were seen in the brains of either species.
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PMID:Toxicity of methylenedioxymethamphetamine (MDMA) in the dog and the rat. 288 76

The effects of 8 imidazoline derivatives on the cardiovascular system and their acute toxicity were investigated. In anesthetized rats, K-6341 and K-6343 produced relatively long-lasting elevation of blood pressure. This hypertensive response was prevented by prazosin. In contrast, K-4011, K-3827 and K-4300 exerted long-lasting hypotensive actions. Norepinephrine-induced increase in blood pressure was competitively antagonized by these three derivatives. Therefore, the hypertensive and hypotensive actions of imidazoline derivatives are conceivably exerted by activating and blocking alpha 1-adrenoceptors. In the isolated guinea-pig atrial preparations, K-4011, K-3827, K-6341 and K-6343 produced positive inotropic responses which were independent of beta-adrenoceptor activation. The positive inotropic effect of K-6341, which was the most potent, was specifically attenuated or abolished by diltiazem, suggesting that a change in Ca2+ movement across the cell membrane is contributing to K-6341-induced increase in atrial contractions. The main symptoms of mice manifested when injected with imidazoline derivatives were a decrease in spontaneous movement, exophthalmos, an increase in palpebral opening, paralysis of four limbs and respiratory depression. Acute LD50 values of imidazoline derivatives in mice (i.v., i.p.) were between these of tolazoline and naphazoline.
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PMID:Pharmacological studies of imidazoline derivatives. III. Actions on cardiovascular system and acute toxicity. 373 60

Twenty-three 2- to 5-month-old Beagle dogs were fed a purified thiamine-deficient ration (2 to 3 micrograms of thiamine/100 g of ration) at a rate of 40 to 70 g/kg of body weight/day depending on age. Eleven dogs were used as principles, 6 as pair-fed controls, and 6 as ad libitum-fed controls. Controls were treated once a week with an IM dose of 300 micrograms of thiamine hydrochloride/kg of body weight. Three stages of clinical disease occurred in the principals: (i) an initial short (18.0 +/- 7.9 days) stage of induction, during which the dogs usually grew suboptimally, but were otherwise healthy, (ii) an intermediate stage of preliminary clinical signs of deficiency, characterized by a variable period (58.5 +/- 37.0 days) of progressive inappetance, failure to grow, loss of body weight, and coprophagia, and (iii) a terminal stage, which, in most dogs, was abrupt in onset and short (7.6 +/- 6.0 days) and consisted of either a neurologic syndrome or sudden unexpected death syndrome. Eight of the principals developed the neurologic syndrome characterized by anorexia, emesis, CNS depression, paraparesis, sensory ataxia, torticollis, circling, exophthalmos, tonic-clonic convulsions, profound muscular weakness, recumbency, and then died. Common reflex abnormalities included exaggerated patella reflex, proprioceptive and supporting reflex deficits, induced torticollis and ventroflexion of head, and absent eye menace (blink) reflex. Three other principals developed the sudden unexpected death syndrome. Common signs of deficiency were inappetance and paresis. Two were found dead and 1, with severe ECG abnormalities (including elevation of ST segment and tall or deeply inverted T waves), was killed.
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PMID:Experimentally induced thiamine deficiency in beagle dogs: clinical observations. 719 32

A clinical study of the craniofacial features in Apert syndrome is based on our experience with 136 cases. Characteristics included hyperacrobrachycephaly, steep wide forehead, flat occiput, common craniofacial asymmetry, ocular hypertelorism and proptosis, downslanting palpebral fissures, divergent upgaze and esotropic downgaze, a tendency towards large ears, and marked depression of the nasal bridge. The nose is short and wide with a bulbous tip, and the anterior facial height is reduced. Common features during infancy included horizontal grooves above the supraorbital ridges that disappear with age, a break in the continuity of the eyebrows, and a trapezoidal-shaped mouth at rest. Radiographic aspects of Apert syndrome were also assessed. Tables are provided which compare the craniofacial features of Apert and Crouzon syndromes.
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PMID:A clinical study of the craniofacial features in Apert syndrome. 883

We report o a baby from an Arab family with Raine syndrome. The baby presented at birth with severe craniofacial anomalies including a wide anterior fontanelle, exophthalmos, severe depression of the nasal bridge with a hypoplastic midface, bilateral choanal atresia and a large protruding tongue. All the limbs were short and the thorax was small. Radiologically there was increased bone density in some bones, periosteal new bone formation and marked bowing of the femurs, tibiae, and ulnae. We suggest that osteosclerosis in Raine syndrome is not necessarily severe and generalized, and bowing of the long bones is another variable radiological feature of the syndrome.
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PMID:Further delineation of Raine syndrome. 1286 69

A method has been described for the study of the central effects produced by the intracerebral injection of drugs in the unanaesthetized mouse. The effects observed were in good agreement with those obtained after similar injections in cats, dogs and human beings. After intracerebral injection, drugs of diverse structure produced certain generalized effects: changes in positioning of the tail, stupor, hyperexcitability and tachypnoea. Both acetylcholine and methacholine produced an akinetic seizure and depression, but the latter compound also caused lacrimation and salivation. Atropine produced piloerection, increased sensitivity to sound and touch, clonic convulsions and scratching, whereas hexamethonium caused Parkinsonian-like muscle tremors and peripheral vasodilatation. After adrenaline, hyperexcitability, exophthalmos, stupor and death from pulmonary oedema were observed, but (+)-methylamphetamine produced only piloerection and exaggerated activity in response to sound and touch. Ergotamine caused a decreased sensitivity to sound and touch, micturition, and stupor, while ergometrine caused clonic convulsions, piloerection, defaecation and stupor.
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PMID:Pharmacological effects produced by intracerebral injection of drugs in the conscious mouse. 1341 44

ABCA5 is a member of the ABC transporter A subfamily, and a mouse orthologue (mABCA5) in newborn mouse brain and neural cells was identified by reverse transcription-PCR. Full-length cDNA cloning revealed that mABCA5 consists of 1,642 amino acid residues and that its putative structure is that of a full-type ABC transporter having two sets of six transmembrane segments and a nucleotide binding domain. Immunohistochemical studies revealed that mABCA5 is expressed in brain, lung, heart, and thyroid gland. A subcellular localization analysis showed that mABCA5 is a resident of lysosomes and late endosomes. Abca5(-)(/)(-) mice exhibited symptoms similar to those of several lysosomal diseases in heart, although no prominent abnormalities were found in brain or lung. They developed a dilated cardiomyopathy-like heart after reaching adulthood and died due to depression of the cardiovascular system. In addition, Abca5(-)(/)(-) mice also exhibited exophthalmos and collapse of the thyroid gland. Therefore, ABCA5 is a protein related to a lysosomal disease and plays important roles, especially in cardiomyocytes and follicular cells.
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PMID:ABCA5 resides in lysosomes, and ABCA5 knockout mice develop lysosomal disease-like symptoms. 1587 Feb 84


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