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

A clinical and neuropsychological syndrome for early recognition of occult hydrocephalus and cerebral atrophy is described. Five illustrative patients are reported. The main features of the syndrome are (i) subjective non-specific complaints (headaches, depression and loss of memory); (ii) the tonic foot response of the sole and the grasp reflex of the foot in the absence of the grasp reflex of the hand; (iii) attacks of sudden and transient loss of muscle tone in both lower limbs leading to falls without warning while standing or while walking. These attacks indistinguishable from drop-attacks are termed chalastic fits; (iv) a dissociation between the satisfactory performances on the Ottawa-Wechsler scale and the poor performances on Kohs Block Design test. Clinical and neuropsychological findings could not differentiate between occult hydrocephalus and cerebral atrophy; only radionuclide cisternography and computerized tomography were able to delineate the final diagnosis.
 ...
PMID:A syndrome of early recognition of occult hydrocephalus and cerebral atrophy. 91 52

The mechanism of action of a carboxypeptidase inhibitor from potatoes has been probed by studying its interaction with derivatives of carboxypeptidase A containing modified residues at the active site. Arsanilazocarboxypeptidase A, a derivative containing a chromophore attached to tyrosine 248, exhibits a circular dichroism spectrum which is sensitive to the presence of ligands at the active site (Kagan, H.M., and Vallee, B.L. (1969), Biochemistry 8, 4223). Since the spectral change attending binding of the carboxypeptidase inhibitor to arsanilazocarboxypeptidase A is similar to that produced by small substrates and inhibitors, the enzyme-inhibitor interaction also involves the enzyme active site. Catalytic activity is not required for inhibitor binding. Complexes of the inhibitor with apocarboxypeptidase A anc carboxypeptidase A which was inactivated by treatment with the affinity label, N-bromoacetyl-N-methyl-L-phenylalanine, are demonstrated by gel filtration experiments. Morever, competitive binding studies reveal that the latter derivative, in which the binding pocket is presumably blocked by reagent, binds inhibitor nearly as strongly as does the native enzyme, and differences in free energy of association being only 0.4 kcal/mol of a total binding energy of - 11 kcal/mol. A model is proposed to account for both the tight binding of inhibitor to the N-bromoacetyl-N-methyl-L-phenylalanine derivative and the involvement of the active site of arsanilazocarboxypeptidase A. It is suggested that the inhibitor fits into a shallow depression at the active site of the enzyme but does not penetrate into the binding pocket.
 ...
PMID:Carboxypeptidase inhibitor from potatoes. Interaction with derivatives of carboxypeptidase A. 93 26

1. The use of Li pre-treatment in rats before high pressure oxygen exposure has been reported effective in controlling convulsions. This is an effect which is better demonstrated if exposure to oxygen follows shortly after Li injection than exposure following several hours later. 2. This study has investigated the hypothesis that the protective action of Li may be exerted, in the short term, by its removing ammonia from the blood and alleviating the latter's known toxic action. 3. A normal Li distribution time profile in unstressed rat brain and blood following intraperitoneal injection has been established. Brain and blood ammonia, amino acids and Li concentrations were also measured in Li-treated animals exposed and convulsed by oxygen. These measurements were made both shortly (15 min) and also several hours after (24 hr) Li treatment. Ammonia and amino acid values in Li-protected groups were compared to normal unstressed animal values and also to values in animals convulsed by oxygen unprotected by Li pre-treatment. 4. In rat brain abd blood significant (P less than 0-001) elevation of ammonia and glutamine and depression of gamma-amino butyric acid (brain only) and glutamate was noted following oxygen treatment in unprotected animals. Prior injection of Li 15 min before high pressure oxygen exposure delayed convulsions twice as long. Additionally if these animals were only exposed to oxygen for a period of time equal to that which would normally produce convulsions in unprotected animals, brain and blood ammonia and amino acids were maintained near to unstressed animal levels. Concomitantly, blood Li concentrations were considerably depressed below the values one would expect from the previously determined Li distribution time profile. 5. In rats exposed to high pressure oxygen 24 hr after Li treatment there was no protective action against high pressure oxygen convulsion, rather a potentiating effect for convulsion was seen. 6. These data present compelling evidence for the controlling effect of Li in rats, on rising blood ammonia concentration which occurs in high pressure oxygen exposure. The effect might well be due to the known chelating properties of Li with ammonia.
 ...
PMID:Lithium protection against oxygen toxicity in rats: ammonia and amino acid metabolism. 97 69

Coptis root is frequently utilized as a sedative in Chinese medicines, however, the central depressant action of this compound has not been reported. Such being the case, the central depressant actions of methanol extract of coptis root, its active ingredients such as non-alkaloids fraction, tertiary base fraction, quarternary base fraction, magnoflorine fraction, berberine hydrochloride, coptisine hydrochloride and the extract from SAN O SHA SHIN TO being one of the preparations which contain coptis root were investigated in mice. The antigastric ulcer action of these substances was also examined in rats. All substances were given orally. Sontaneous movement and coordinative motor activity were not depressed by methanol extract, non-alkaloid fraction quarternary base fraction, magnoflorine fraction, berberine hydrochloride, coptisine hhdrochloride and the extract from SAN O SHA SHIN TO. There was no inhibition of chemical- and electro-shock-induced convulsion, morphine induced Straub's tail reaction, apomorphine-induced masticating motion and aggressive behavior induced by electrical stimulation. A loss of righting reflex due to hypnotics was not potentiated by the substances. The quarternary base fraction did not elicit central depression, while the tertiary base fraction slightly depressed the function of the central nervous system. Quarternary base alkaloids such as berberine exerted a slight antiulcer effect.
 ...
PMID:[Behavioral pharmacology of berberine-type alkaloids. (1) Central depressive action of Coptidis rhizoma and its constituents]. 103 91

The case report of the corticosteroid complication in an eight-year-old girl with immune thrombocytopenic purpura is presented. She was treated with high dosage corticosteroids and incurred severe side effects, including bone marrow depression, renal magnesium stones, osteoporosis, depression of affect, convulsions with cerebral damage and adrenal suppression.
 ...
PMID:Unwanted corticosteroid effects in childhood bone marrow failure, renal failure and brain damage: case report. 105 40

Allergies of the nervous system cause diverse behavioral disturbances, including headaches, convulsions, learning disabilities, schizophrenia and depression. Some of the biological mechanisms have been established by research; others remain to be explored. Effective diagnosis and treatment include the elimination diet, followed by dietary rotation and avoidance of offending substances.
 ...
PMID:Allergy of the nervous system: a review. 110 12

Impact between the brain and the cristae of the base normally results as a consequence of inertia when an obstacle is hit, followed by contusion, or intra-, sub- or extradural haematoma. The skull itself may be briken (usually at the interpilasters or the weak points of the pilasters) or dented. Denting resulted in the depression of a circular fragments or fragments, with compression of the dura mater or brain; this, in turn, may be contused, lacerated or even crushed. Spinal crash fractures usually involve the lumbar region. Neck fractures are rare. The picture may be one of clinical silence (local pain) or marked neurological involvement. Damage to the cord is expressed in the form of shock, complete flaccid para- or tetraplegia, complete loss of sensation below the lesion, loss of deep and superficial reflexes, urinary retention and rectal incontinence. Treatment is rendered complicated by profuse scalp haemorrhages, respiratory insufficiency requiring orotracheal intubation and assisted respiration, convulsions, which should be handled with care, since ordinary anti-epilepsy products may mask the onset of hypertension and haematoma. Swelling should be reduced with cortisones. Diuretics may be too brusque and lead to intracerebral haematoma. In the case of spinal injuries, particular care should be excercised in shifting the patient and conveying him to hospital. Where high neck lesions are suspected, the possibility of damage to the originating segments of the phrenic nerve must be borne in mind.
 ...
PMID:[Aeromedical problems in cranio-vertebral injuries]. 112 65

Atropine (At) and scopolamine (Sc) in low doses intensify basic activity, increase amphetamine stereotypy, and suppress catalepsy induced by injection of haloperidol. High doses lower body temperature, antagonize amphetamine stereotypy, and intensify the hypnotic action of chloral hydrate. Doses of about 1/2 LD50 induce narcotic sleep. Both At and Sc in a wide range of dosage protect against the tonic phase of convulsions produced by electroshock. Sc depresses content of acetylcholine in the brain proportionally to its dosage; At had a similar effect only at the lower of the two doses that were used. Both compounds had no effect on levels of noradrenaline and dopamine in the brain. The results indicate that low doses of blockers of the cholinergic muscarinic receptor, injected intraventricularly, produce strong central stimulation, whereas high doses produce depression of the central nervous system.
 ...
PMID:Central action of drugs acting on the cholinergic muscarinic receptor. III. Influence of atropine and scopolamine injected intraventricularly on behavior and levels of biogenic amines in the rat brain. 117 21

The development of behavioral sensitivity to strychnine has been studied in the chick embryo between day 7 of incubation and 1 day posthatching. The earliest response to systemically applied strychnine was a marked depression of spontaneous motility at high concentrations of the drug. Lower concentrations had no effect at this time (6-7 days). About 2 days later, on day 81/2 or 9, strychnine induced a statistically reliable increase in spontaneous motility (hyperactivity). This consisted of a brief (i.e. 1-2 min) excitatory response which was followed by a return to baseline activity levels in the case of low drug concentrations, or a depression of activity in the case of low drug concentrations, or a depression of activity in the case of higher concentrations. By 11 days of incubation the brief excitatory response following strychnine had increased in duration to about 4 min. This was also the case for 13-day embryos. At no time between 7 and 13 days were convulsions produced by strychnine, even at concentrations several times greater than that required to induce hyperactivity. For the first time at 16 days myoclonic convulsions were observed following strychnine. These usually began soon after the initial hyperactivity and frequently lasted for as long as 30 min. At the same time the sensitivity of the embryo to strychnine increased, compared to earlier stages. By 18 days strychnine most often induced an immediate convulsive response without the preceding brief hyperactivity. This was also typical of newly hatched chicks. The systemic application of glycine at 9 and 13 days of incubation produced a slight, but statistically reliable, depression of ongoing spontaneous motility, consistent with what one might expect if glycine were acting as an inhibitory neurotransmitter. It typically took between 3 and 4 min following injection for this glycine response to occur. Biochemical, electrophysiological and neuroanatomical evidence was reviewed in an attempt to support the suggestion that the strychnine and glycine data summarized above may reflect the presence of strychnine-sensitive postsynaptic inhibitory processes in the chick spinal cord. Additionally, comparative data on the relative onset of excitatory and inhibitory processes in the developing spinal cord were discussed. It was concluded that, although the data are still imcomplete concerning the question of whether, developmentally, inhibition is a primary or secondary acquisition, inhibitory mechanisms nevertheless appear rather early during vertebrate neurogenesis.
 ...
PMID:Ontogeny of behavioral sensitivity to strychnine in the chick embryo: evidence for the early onset of CNS inhibition. 117 33

Microiontophoretic administrations of morphine to cholino-excitable neurones in the cerebral cortex of decerebrate cats evoked a weak excitation which became more prominent upon repeated administrations of the alkaloid. This effect was not antagonized by naloxone. Iontophoresis of methylatropine prevented the excitation induced with acetylcholine and morphine, leaving that caused by glutamate relatively unaltered. Similar applications of morphine to neurones which were not excited by test applications of acetylcholine did not result in excitation but elicited mainly a depression of glutamate-evoked firing. It is suggested that the muscarinic effect of morphine in the cortex may be related to the excitation and convulsions, but not the analgesia, which occurs upon systemic administrations of the narcotic.
 ...
PMID:Morphine excitation in the cerebral cortex. 117 94


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>