UMLS:C0011570 - FACTA Search

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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Persistent bleeding from the vulva was the only presenting clinical sign in five non-pregnant pluriparous mares varying in age from eight to 20 years. These were two hunter types, one shire, one thoroughbred and one Arab pony. The haemorrhage originated from ulcerated varicose veins present on the dorsal wall of the vagina adjacent to the vestibulovaginal junction. All five mares were successfully treated, by submucosal resection (two), ligation of vessels (two) or diathermy (one). In four mares there was evidence of vulval incompetence caused by depression of the perineum. The importance of this and the role of impaired venous return during and after pregnancy are discussed.
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PMID:Persistent vaginal haemorrhage in five mares caused by varicose veins of the vaginal wall. 649 76

Two groups of six patients were studied during light general anaesthesia using 2% enflurane and 66% nitrous oxide in oxygen, combined with regional anaesthesia, for hernia and varicose vein surgery. The effects of 3% enflurane were compared with those of fentanyl 0.3 microgram kg-1 i.v., by measuring inspired flow, tidal volume, the timing of inspiration and expiration, and occlusion pressure. Three per cent enflurane decreased ventilation by 12%. Tidal volume, mean inspiratory flow and occlusion pressure were decreased in approximately equal proportions (14, 12 and 8%, respectively). The timing of breathing did not change significantly. Fentanyl did not influence tidal volume. Ventilation was decreased by 28% as a result of a 10% decrease in inspiratory flow and a marked increase in the duration of expiration by 45%. The pattern of activation of the inspiratory muscles, as indicated by occlusion pressure, was changed by fentanyl. During enflurane and nitrous oxide anaesthesia, depression of ventilation by fentanyl or increases in enflurane concentration was not by a common central depressant mechanism.
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PMID:Comparison of decreases in ventilation caused by enflurane and fentanyl during anaesthesia. 661 70

Oral contrceptives (OCs), usd by over 30% of reproductive aged women in Belgium, are by far the most widely used contraceptive in that country. The various types of OCs include monophasic, biphasic, and triphasic combinations of an estrogen and a progestin, sequentials containing estrogen only for 7-14 days followed by a progestin through the 21st day; macrodose or microdose progestin only formulations, 3-month injectable progestins, and the morning after pill. Side effects of OCs are mainly due to metabolic effects on coagulation factors, the renin-angiotensin system, glucose tolerance, or the lipid profile. Users of OCs face increased risks of cholelithiases, thrombophlebitis, thromboembolism, cerebrovascular accidents, myocardial infarcts (among smokers over 35 years of age), and hepatic adenomas. The most troubling secondary effect is the excess cardiovascular morbidity and mortality show by contraceptive users, not just those who are obese, hypertensive, or who have histories of vascular pathology, but also those over 40 years of age and smokers. Lenght of use of OCs does not increase vascular risks. Epidemiologic studies demonstrate that vascular risks are reduced in lower dose formulations. Absolute contraindications to OC use include serious cardiovascular problems, severe hepatic pathology, estrogen-dependent tumors, pregnancy and undiagnosed gynecologic problems, and significant hyperlipidemia. Relative contraindications include severe headaches, cholelithiase, previous cholestasis of pregnancy, severe renal disease, fibromyomas, benign breast disease, age over 40 years, smoking, surgery anticipated within 4 weeks, infectious mononucleosis, falciform anemia, and immediate postpartum and lactation. Epilepsy, diabetes, depression, and varicose veins are not strictly speaking contraindications but require additonal surveillance. Lower dose formulations should be prescribed if possible. OC users should be followed up every 6-12 months. Among other steroidal contraceptive methods, sequential OCs and high dose progestin-only formulations are used for short-term treatment of specific conditions. Progestin-only minipills are used when an OC is desired but estrogens are contraindicated. Injectable progestins should be reserved for patients who for cultural or medical reasons can use no other type of contraceptive. Morning-after pills should not be considered a regular form of contraception. If OCs are used in adolescents, a low dose pill is indicated. Low dose OCs may be indicated for diabetics because of the danger of infection with IUDs and the lesser efficacy of barrier methods. If OCs are used in epileptics, they should be regular dosed because of the danger of drug interactions. Only low-dose formulations and progestin-only minipills should be used by women over 40.
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PMID:[The choice of oral contraception in 1984: general indications and specific cases]. 672 93

1. The myenteric plexus-longitudinal muscle preparation of the guinea-pig ileum was incubated with [(3)H]choline (1.125-1.5 muM), and then superfused with Tyrode solution containing hemicholinium-3 (10 muM). Secretion of [(3)H]acetylcholine ([(3)H]ACh) was evoked either (a) by electrical field stimulation (0.5-15 Hz, 150 shocks per period, 0.5 msec), used to ;indirectly' depolarize the varicosities of nerve terminals, or (b) by high potassium (40 mM with 1 muM-tetrodotoxin, for 6 min, or 80 mM without tetrodotoxin, for 1 min), to ;directly' depolarize varicosities.2. With these stimulation parameters, which yielded about the same fractional secretion of [(3)H]ACh, and with eserine (10 muM) present in the medium, atropine (1 muM) enhanced the ;indirectly', electrically evoked secretion 3.65+/-0.34 (n = 6) fold, and that caused by 40 mM or 80 mM-potassium 1.82+/-0.06 (n = 6) or 1.55+/-0.09 (n = 10) fold, respectively. Atropine thus enhanced ;indirectly', electrically evoked secretion 4-fold more than that caused by ;direct' depolarization of varicosities with high potassium (P < 0.001).3. This difference is not likely to be caused by depression of the sensitivity of the presynaptic muscarinic receptors to ACh released by nerve stimulation, caused by the hypertonicity of the medium in the potassium stimulation experiments. The medium made hypertonic by addition of Tris-HEPES (80 mM) did lower the binding affinity of membrane preparations of (pre- and post-synaptic) muscarinic receptors, to carbamylcholine, and also the contractile responsiveness of the longitudinal muscle to this agent, in both cases to about one half. But it did not appear to alter the responsiveness of either pre- or post-synaptic muscarinic receptors to endogenous ACh, released by nerve stimulation.4. The results support a dual-mode model for the muscarinic negative feed-back control of ACh secretion from the nerve terminals of this preparation, mainly operating by restriction of the invasion of terminals, and only secondarily by depression of the efficiency of depolarization-secretion coupling in invaded varicosities.5. Since this model has earlier been proposed to apply for the control of secretion of [(3)H]noradrenaline from the micro-anatomically similar nerve terminals of noradrenergic nerves, the present findings suggest that the model may have a wider biological significance, and possibly apply to the control of the secretory activity of boutons-en-passant nerve terminals in general.
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PMID:The effects of atropine on [3H]acetylcholine secretion from guinea-pig myenteric plexus evoked electrically or by high potassium. 714 61

5-HT or FMRFamide evoke long-lasting changes in the efficacy of sensorimotor (SN-L7) synapses of Aplysia, structural alterations of the presynaptic sensory cell, and cell-specific downregulation in the distribution of the adhesion molecule apCAM. We examined how the cell-specific changes in apCAM might contribute to the formation of new presynaptic varicosities by 5-HT or the elimination of existing presynaptic varicosities by FMRFamide. We report that the formation of new sensory varicosities is directed by the presence of preexisting zones on the motor axon that are enriched for apCAM. Moreover, there was a further enrichment of apCAM levels at existing sensory varicosities contacting the motor axon beginning at 1 hr and lasting 24 hr after treatment with 5-HT. As was found for synapse formation during the early stages of cell-cell interaction, incubation with anti-apCAM mAb blocked the 5-HT-induced long-term changes in synaptic efficacy and the accompanying changes in sensory neuron structure. Long-term synaptic depression with FMRFamide was accompanied by an overall decline of apCAM levels. Treatment with FMRFamide evoked an even greater decline in apCAM levels at sites of sensory varicosities that preceded the structural changes and persisted especially at sites where sensory varicosities are eliminated. These results suggest that neurotransmitters evoke both cell- and site-specific changes in the levels of adhesion molecules that can influence either the formation or the elimination of presynaptic varicosities that accompany long-term heterosynaptic modulation of a behaviorally relevant synaptic connection.
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PMID:Changes in expression and distribution of Aplysia cell adhesion molecules can influence synapse formation and elimination in vitro. 779 Sep 3

1 Transmitter release from sympathetic varicosities of mouse vasa deferentia removed from animals which were chronically treated with morphine for 7 to 9 days has been evaluated. 2 In control preparations increasing the extracellular calcium concentration ([Ca2+]o) from 1 to 2 mM increased transmitter release by 3 fold while increasing [Ca2+]o from 6 to 8 mM increased transmitter release by about 0.9 fold. Introduction of morphine (1.0 microM) produced a uniform decrease in transmitter release, shifting the relationship between transmitter release and [Ca2+]o to the right. 3 Only sympathetic varicosities with probabilities of transmitter release greater than 0.01 were chosen for this study. In these varicosities the decrease in transmitter release induced by morphine in control preparations (bathed in [Ca2+]o 2.0 mM) was not observed following 7 to 9 days of morphine treatment. When the morphine was acutely withdrawn from these preparations transmitter release was more than 6 times the average level of transmitter release from control preparations. 4 The morphine induced increase in facilitation of transmitter release while stimulating with short trains of nerve impulses was not observed when the preparations were removed from animals which had been exposed to morphine for 7 to 9 days. When these preparations were acutely withdrawn from morphine there was a further decrease in the level of facilitation and a significant increase in depression of transmitter release when compared to control. 5 The morphine induced decrease in probability of transmitter release when naive sympathetic varicosities in vitro were bathed with morphine (1 microM) was not observed following chronic morphine treatment of the animals for 7 to 9 days. When the morphine was acutely withdrawn from chronically morphine treated preparations the underlying increase in probabilities of transmitter release of sympathetic varicosities was unmasked.
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PMID:Effect of chronic morphine treatment on transmitter release from sympathetic varicosities of the mouse vas deferens. 868 Jul 17

Because no contraceptive agent is perfect, patients must weigh the benefits and risks of the contraceptive method they decide to initiate and continue. Individual decision making and provider-client communication interact in complex ways to determine contraceptive behavior. Use of the contraceptive injectable depot medroxyprogesterone acetate (DMPA) should be preceded by counseling which individualizes its risks and benefits, answers all questions (asked and unasked), and develops a longterm plan to minimize side effects. Counseling should cover the contraceptive and noncontraceptive benefits of DMPA; specific side effects such as bleeding changes, weight changes, and fertility changes; the mechanisms of action; and ways to avoid acquiring sexually transmitted diseases. When evaluating and managing side effects, a differential diagnosis independent of DMPA must be considered first (especially for postcoital bleeding and headache). A pregnancy test should be offered in the first month of amenorrhea, after which no treatment is necessary. Ovulation resumption after use may be spontaneous or may be induced with menotropin therapy. Spotting and breakthrough bleeding may be handled by counseling or by a short course of high-dosage ibuprofen or of low-dose estrogen supplementation. Counseling may help women manage weight gain through caloric reduction and an increase in exercise. Acne which occurs soon after adoption of the method may be managed pharmacologically. Increased intake of dietary fiber and fluids may ameliorate the symptoms of abdominal bloating, and temporary nausea can be treated with antacids. Recent research has shown that depression does not increase with DMPA use, although the contraceptive is sometimes implicated in mood changes. Breast tenderness decreases with prolonged DMPA usage and can be managed with proper support garments and a reduction in other causative agents such as caffeine. Women who experience an increase in varicose veins should wear support hose and elevate their legs when possible. Women with symptoms of hypoestrogenic side effects should undergo a serum estradiol level test and appropriate replacement therapy. DMPA can be used immediately postpartum even in breast-feeding women. Women with amenorrhea should be tested for pregnancy before initiating DMPA or reinitiating use at an interval longer than 11-13 weeks. No adverse side effects have been found if pregnancy does occur.
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PMID:Counseling issues and management of side effects for women using depot medroxyprogesterone acetate contraception. 872 1

The synapses between the sensory neuron (SN) and motor neuron of Aplysia undergo long-term functional and structural modulation with appropriate behavioral training or with applications of specific neuromodulators. Expression of molecules within the presynaptic terminals may be regulated in parallel with the changes evoked by the neuromodulators. We examined with immunocytochemical methods whether the level of sensorin, the SN-specific neuropeptide, is modulated in SN varicosities by the location of interaction with the target motor cell L7 and by applications of either 5-HT that evoke long-term facilitation or FMRFamide that evoke long-term depression of Aplysia sensorimotor connections in vitro. A significantly higher proportion of SN varicosities are sensorin positive when they are in contact with the proximal axons of L7 compared to varicosities of the same SNs in contact with distal L7 neurites. Both 5-HT and FMRFamide evoked changes in the efficacy and structure of sensorimotor connections that are accompanied by changes in the frequency of sensorin-positive varicosities contacting the axons of L7. More preexisting SN varicosities are stained after 5-HT, and fewer preexisting SN varicosities are stained after FMRFamide. These results suggest that the postsynaptic target and the neuromodulators not only regulate overall structure but also regulate the level of SN neuropeptide at synaptic sites.
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PMID:Neuropeptide localization in varicosities of Aplysia sensory neurons is regulated by target and neuromodulators evoking long-term synaptic plasticity. 891 Jul 88

Many neuromodulators inhibit N-type Ca2+ currents via G protein-coupled pathways in acutely isolated superior cervical ganglion (SCG) neurons. Less is known about which neuromodulators affect release of norepinephrine (NE) at varicosities and terminals of these neurons. To address this question, we used carbon fiber amperometry to measure catecholamine secretion evoked by electrical stimulation at presumed sites of high terminal density in cultures of SCG neurons. The pharmacological properties of action potential-evoked NE release paralleled those of N-type Ca2+ channels: Release was completely blocked by Cd2+ or omega-conotoxin GVIA, reduced 50% by 10 microM NE or 62% by 2 microM UK-14,304, an alpha2-adrenergic agonist, and reduced 63% by 10 microM oxotremorine M (Oxo-M), a muscarinic agonist. Consistent with action at M2 or M4 receptor subtypes, Oxo-M could be antagonized by 10 microM muscarinic antagonists methoctramine and tropicamide but not by pirenzepine. After overnight incubation with pertussis toxin, inhibition by UK-14,304 and Oxo-M was much reduced. Other neuromodulators known to inhibit Ca2+ channels in these cells, including adenosine, prostaglandin E2, somatostatin, and secretin, also depressed secretion by 34-44%. In cultures treated with omega-conotoxin GVIA, secretion dependent on L-type Ca2+ channels was evoked with long exposure to high K+ Ringer's solution. This secretion was not sensitive to UK-14,304 or Oxo-M. Evidently, many neuromodulators act on the secretory terminals of SCG neurons, and the depression of NE release at terminals closely parallels the membrane-delimited inhibition of N-type Ca2+ currents in the soma.
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PMID:Modulation by neurotransmitters of catecholamine secretion from sympathetic ganglion neurons detected by amperometry. 903 83

The serotonin (5-HT) transporter (5-HTT) is known to play a role in depression and many 5-HT related diseases, and is the target site for drugs of abuse, such as cocaine, MDMA, and methamphetamine. The major role of the 5-HTT has long been considered to be to inactivate serotonin transmission through the elimination of serotonin at release sites. However, immunocytochemistry using an antibody against the N-terminal of the 5-HTT at the light microscopic (LM) level indicates that the 5-HTT is associated not only with 5-HT varicosities but also with axons. Electron microscopy (EM) reveals that the majority of the 5-HTTs exist on the axolemma outside the synaptic junctions. In studying whether axonal 5-HTTs are involved in the uptake of 5-HT, we found with autoradiography that [3H]citalopram bound to all major 5-HT fibers, not only in the terminal regions, but also in 5-HT axonal bundles such as the cingulum bundle and medial forebrain bundle. Furthermore, voltammetry recordings indicated that serotonin axonal bundles were actively engaged in high affinity serotonin uptake. The evidence indicates that 5-HTTs on 5-HT axons away from the synapse are likely to be functional in a manner similar to the terminal 5-HTT for serotonin uptake. It also suggests that the role of the 5-HTT may not only be for the termination of synaptic transmission, but also for the regulation of 5-HT through extrasynaptic (volume) transmission. Our findings may also impact the understanding of the sites of action of selective serotonin reuptake inhibitors and drug entry into serotonin neurons via the numerous axonal sites.
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PMID:Serotonin transporters are located on the axons beyond the synaptic junctions: anatomical and functional evidence. 973 75

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