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Showing 37 to 48 of 1115 entries
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Mannich bases: an important pharmacophore in present scenario.

International journal of medicinal chemistry

Bala S, Sharma N, Kajal A, Kamboj S, Saini V.
PMID: 25478226
Int J Med Chem. 2014;2014:191072. doi: 10.1155/2014/191072. Epub 2014 Nov 12.

Mannich bases are the end products of Mannich reaction and are known as beta-amino ketone carrying compounds. Mannich reaction is a carbon-carbon bond forming nucleophilic addition reaction and is a key step in synthesis of a wide variety of...

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Bala S, Sharma N, Kajal A, et al. Mannich bases: an important pharmacophore in present scenario. Int J Med Chem. 2014;2014:191072doi: 10.1155/2014/191072.
Bala, S., Sharma, N., Kajal, A., Kamboj, S., & Saini, V. (2014). Mannich bases: an important pharmacophore in present scenario. International journal of medicinal chemistry, 2014191072. https://doi.org/10.1155/2014/191072
Bala, Suman, et al. "Mannich bases: an important pharmacophore in present scenario." International journal of medicinal chemistry vol. 2014 (2014): 191072. doi: https://doi.org/10.1155/2014/191072
Bala S, Sharma N, Kajal A, Kamboj S, Saini V. Mannich bases: an important pharmacophore in present scenario. Int J Med Chem. 2014;2014:191072. doi: 10.1155/2014/191072. Epub 2014 Nov 12. PMID: 25478226; PMCID: PMC4244926.
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Resveratrol increases F508del-CFTR dependent salivary secretion in cystic fibrosis mice.

Biology open

Dhooghe B, Bouckaert C, Capron A, Wallemacq P, Leal T, Noel S.
PMID: 26092868
Biol Open. 2015 Jun 19;4(7):929-36. doi: 10.1242/bio.010967.

Cystic fibrosis (CF) is a fatal genetic disease associated with widespread exocrine gland dysfunction. Studies have suggested activating effects of resveratrol, a naturally-occurring polyphenol compound with antioxidant and anti-inflammatory properties, on CF transmembrane conductance regulator (CFTR) protein function. We...

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Dhooghe B, Bouckaert C, Capron A, et al. Resveratrol increases F508del-CFTR dependent salivary secretion in cystic fibrosis mice. Biol Open. 2015;4(7):929-36doi: 10.1242/bio.010967.
Dhooghe, B., Bouckaert, C., Capron, A., Wallemacq, P., Leal, T., & Noel, S. (2015). Resveratrol increases F508del-CFTR dependent salivary secretion in cystic fibrosis mice. Biology open, 4(7), 929-36. https://doi.org/10.1242/bio.010967
Dhooghe, Barbara, et al. "Resveratrol increases F508del-CFTR dependent salivary secretion in cystic fibrosis mice." Biology open vol. 4,7 (2015): 929-36. doi: https://doi.org/10.1242/bio.010967
Dhooghe B, Bouckaert C, Capron A, Wallemacq P, Leal T, Noel S. Resveratrol increases F508del-CFTR dependent salivary secretion in cystic fibrosis mice. Biol Open. 2015 Jun 19;4(7):929-36. doi: 10.1242/bio.010967. PMID: 26092868; PMCID: PMC4571083.
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New onset refractory status epilepticus as an unusual presentation of a suspected organophosphate poisoning.

Case reports in emergency medicine

Waheed S, Sabeen A, Ullah Khan N.
PMID: 25580311
Case Rep Emerg Med. 2014;2014:676358. doi: 10.1155/2014/676358. Epub 2014 Dec 17.

New onset refractory status epilepticus (NORSE) is a new entity in medical literature. It has different infectious and noninfectious etiologies showing a devastating impact onto the clinical outcome of patients. Therapy with anaesthetic and antiepileptic agents often fails to...

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Waheed S, Sabeen A, Ullah Khan N. New onset refractory status epilepticus as an unusual presentation of a suspected organophosphate poisoning. Case Rep Emerg Med. 2014;2014:676358doi: 10.1155/2014/676358.
Waheed, S., Sabeen, A., & Ullah Khan, N. (2014). New onset refractory status epilepticus as an unusual presentation of a suspected organophosphate poisoning. Case reports in emergency medicine, 2014676358. https://doi.org/10.1155/2014/676358
Waheed, Shahan, et al. "New onset refractory status epilepticus as an unusual presentation of a suspected organophosphate poisoning." Case reports in emergency medicine vol. 2014 (2014): 676358. doi: https://doi.org/10.1155/2014/676358
Waheed S, Sabeen A, Ullah Khan N. New onset refractory status epilepticus as an unusual presentation of a suspected organophosphate poisoning. Case Rep Emerg Med. 2014;2014:676358. doi: 10.1155/2014/676358. Epub 2014 Dec 17. PMID: 25580311; PMCID: PMC4281438.
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Effects of Putative Neurotransmitters of the Carotid Body on its Own Glomus Cells.

The European journal of neuroscience

Eyzaguirre C, Monti-Bloch L, Woodbury JW.
PMID: 12106105
Eur J Neurosci. 1990 Jan;2(1):77-88. doi: 10.1111/j.1460-9568.1990.tb00383.x.

Carotid body glomus cells produce and release acetylcholine (ACh), catecholamines, and neuropeptides, and there is biochemical evidence that these cells possess receptors for these substances. Thus, we studied the effects of cholinergics [ACh, nicotine (Nic), bethanechol (BN)] and peptides...

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Eyzaguirre C, Monti-Bloch L, Woodbury JW. Effects of Putative Neurotransmitters of the Carotid Body on its Own Glomus Cells. Eur J Neurosci. 1990;2(1):77-88doi: 10.1111/j.1460-9568.1990.tb00383.x.
Eyzaguirre, C., Monti-Bloch, L., & Woodbury, J. W. (1990). Effects of Putative Neurotransmitters of the Carotid Body on its Own Glomus Cells. The European journal of neuroscience, 2(1), 77-88. https://doi.org/10.1111/j.1460-9568.1990.tb00383.x
Eyzaguirre, C., et al. "Effects of Putative Neurotransmitters of the Carotid Body on its Own Glomus Cells." The European journal of neuroscience vol. 2,1 (1990): 77-88. doi: https://doi.org/10.1111/j.1460-9568.1990.tb00383.x
Eyzaguirre C, Monti-Bloch L, Woodbury JW. Effects of Putative Neurotransmitters of the Carotid Body on its Own Glomus Cells. Eur J Neurosci. 1990 Jan;2(1):77-88. doi: 10.1111/j.1460-9568.1990.tb00383.x. PMID: 12106105.
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Derangement of autonomic nerve control in rat with right ventricular failure.

Pathophysiology : the official journal of the International Society for Pathophysiology

Sanyal SN, Ono K.
PMID: 12039652
Pathophysiology. 2002 Jun;8(3):197-203. doi: 10.1016/s0928-4680(02)00002-0.

The effects of right ventricular hypertrophy and eventual right ventricular failure on autonomic nerve regulation of heart rate variability were investigated using rats with monocrotaline (MCT)-induced pulmonary hypertension. ECG signals were obtained from a radio transmitter placed into the...

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Sanyal SN, Ono K. Derangement of autonomic nerve control in rat with right ventricular failure. Pathophysiology. 2002;8(3):197-203doi: 10.1016/s0928-4680(02)00002-0.
Sanyal, S. N., & Ono, K. (2002). Derangement of autonomic nerve control in rat with right ventricular failure. Pathophysiology : the official journal of the International Society for Pathophysiology, 8(3), 197-203. https://doi.org/10.1016/s0928-4680(02)00002-0
Sanyal, S N., and Ono, K. "Derangement of autonomic nerve control in rat with right ventricular failure." Pathophysiology : the official journal of the International Society for Pathophysiology vol. 8,3 (2002): 197-203. doi: https://doi.org/10.1016/s0928-4680(02)00002-0
Sanyal SN, Ono K. Derangement of autonomic nerve control in rat with right ventricular failure. Pathophysiology. 2002 Jun;8(3):197-203. doi: 10.1016/s0928-4680(02)00002-0. PMID: 12039652.
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Can Patients Safely Undergo Electroconvulsive Therapy While Receiving Monoamine Oxidase Inhibitors?.

Convulsive therapy

Freese KJ.
PMID: 11940823
Convuls Ther. 1985;1(3):190-194.

A review of the experience of monoamine oxidase inhibitors (MAOI) and anesthesia finds few well-documented complications, although theoretic risks of cardiovascular reactions are discussed. Laboratory studies and actual case experiences of patients treated with electroconvulsive therapy (ECT) and MAOI...

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Freese KJ. Can Patients Safely Undergo Electroconvulsive Therapy While Receiving Monoamine Oxidase Inhibitors?. Convuls Ther. 1985;1(3):190-194
Freese, K. J. (1985). Can Patients Safely Undergo Electroconvulsive Therapy While Receiving Monoamine Oxidase Inhibitors?. Convulsive therapy, 1(3), 190-194.
Freese, Kenneth J.. "Can Patients Safely Undergo Electroconvulsive Therapy While Receiving Monoamine Oxidase Inhibitors?." Convulsive therapy vol. 1,3 (1985): 190-194.
Freese KJ. Can Patients Safely Undergo Electroconvulsive Therapy While Receiving Monoamine Oxidase Inhibitors?. Convuls Ther. 1985;1(3):190-194. PMID: 11940823.
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Clinical, cardiopulmonary, hematological and serum biochemical effects of sevoflurane and isoflurane anesthesia in oxygen under spontaneous breathing in sheep.

Small ruminant research : the journal of the International Goat Association

Hikasa Y, Saito K, Takase K, Ogasawara S.
PMID: 10781740
Small Rumin Res. 2000 Jun 01;36(3):241-249. doi: 10.1016/s0921-4488(99)00121-2.

Effects of sevoflurane and isoflurane anesthesia in oxygen on clinical, cardiopulmonary, hematological, and serum biochemical findings were compared in sheep breathing spontaneously undergoing minor surgical operations during short-term (60-80min) or long-term (3-4h) anesthesia. All sheep were premedicated with atropine...

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Hikasa Y, Saito K, Takase K, et al. Clinical, cardiopulmonary, hematological and serum biochemical effects of sevoflurane and isoflurane anesthesia in oxygen under spontaneous breathing in sheep. Small Rumin Res. 2000;36(3):241-249doi: 10.1016/s0921-4488(99)00121-2.
Hikasa, Y., Saito, K., Takase, K., & Ogasawara, S. (2000). Clinical, cardiopulmonary, hematological and serum biochemical effects of sevoflurane and isoflurane anesthesia in oxygen under spontaneous breathing in sheep. Small ruminant research : the journal of the International Goat Association, 36(3), 241-249. https://doi.org/10.1016/s0921-4488(99)00121-2
Hikasa, et al. "Clinical, cardiopulmonary, hematological and serum biochemical effects of sevoflurane and isoflurane anesthesia in oxygen under spontaneous breathing in sheep." Small ruminant research : the journal of the International Goat Association vol. 36,3 (2000): 241-249. doi: https://doi.org/10.1016/s0921-4488(99)00121-2
Hikasa Y, Saito K, Takase K, Ogasawara S. Clinical, cardiopulmonary, hematological and serum biochemical effects of sevoflurane and isoflurane anesthesia in oxygen under spontaneous breathing in sheep. Small Rumin Res. 2000 Jun 01;36(3):241-249. doi: 10.1016/s0921-4488(99)00121-2. PMID: 10781740.
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A comparison of propofol and ketamine/midazolam for intravenous sedation of children.

Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies

Seigler RS, Avant MG, Gwyn DR, Lynch AL, Golding EM, Blackhurst DW, Wilfong DK.
PMID: 12797883
Pediatr Crit Care Med. 2001 Jan;2(1):20-23. doi: 10.1097/00130478-200101000-00005.

OBJECTIVE: To compare ketamine and propofol sedation in children undergoing diagnostic and therapeutic procedures. DESIGN: Retrospective study. SETTING: A six-bed pediatric intensive care unit and a pediatric hematology oncology clinic. PATIENTS: From 1996 to 1998, 405 procedures were performed...

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Seigler RS, Avant MG, Gwyn DR, et al. A comparison of propofol and ketamine/midazolam for intravenous sedation of children. Pediatr Crit Care Med. 2001;2(1):20-23doi: 10.1097/00130478-200101000-00005.
Seigler, R. S., Avant, M. G., Gwyn, D. R., Lynch, A. L., Golding, E. M., Blackhurst, D. W., & Wilfong, D. K. (2001). A comparison of propofol and ketamine/midazolam for intravenous sedation of children. Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies, 2(1), 20-23. https://doi.org/10.1097/00130478-200101000-00005
Seigler, Robert S., et al. "A comparison of propofol and ketamine/midazolam for intravenous sedation of children." Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies vol. 2,1 (2001): 20-23. doi: https://doi.org/10.1097/00130478-200101000-00005
Seigler RS, Avant MG, Gwyn DR, Lynch AL, Golding EM, Blackhurst DW, Wilfong DK. A comparison of propofol and ketamine/midazolam for intravenous sedation of children. Pediatr Crit Care Med. 2001 Jan;2(1):20-23. doi: 10.1097/00130478-200101000-00005. PMID: 12797883.
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The interaction between atropine sulphate and a proteolipid from cerebral cortex studied by light scattering.

FEBS letters

De Robertis E, Gonzalez-Rodriguez J, Teller DN.
PMID: 11947130
FEBS Lett. 1969 Jul;4(1):4-8. doi: 10.1016/0014-5793(69)80180-8.

No abstract available.

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De Robertis E, Gonzalez-Rodriguez J, Teller DN. The interaction between atropine sulphate and a proteolipid from cerebral cortex studied by light scattering. FEBS Lett. 1969;4(1):4-8doi: 10.1016/0014-5793(69)80180-8.
De Robertis, E., Gonzalez-Rodriguez, J., & Teller, D. N. (1969). The interaction between atropine sulphate and a proteolipid from cerebral cortex studied by light scattering. FEBS letters, 4(1), 4-8. https://doi.org/10.1016/0014-5793(69)80180-8
De Robertis, E, et al. "The interaction between atropine sulphate and a proteolipid from cerebral cortex studied by light scattering." FEBS letters vol. 4,1 (1969): 4-8. doi: https://doi.org/10.1016/0014-5793(69)80180-8
De Robertis E, Gonzalez-Rodriguez J, Teller DN. The interaction between atropine sulphate and a proteolipid from cerebral cortex studied by light scattering. FEBS Lett. 1969 Jul;4(1):4-8. doi: 10.1016/0014-5793(69)80180-8. PMID: 11947130.
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Long-lasting depolarization of leech neurons mediated by receptors with a nicotinic binding site.

The Journal of experimental biology

Szczupak L, Edgar J, Peralta ML, Kristan WB.
PMID: 9600871
J Exp Biol. 1998 May 21;201:1895-906.

The serotonergic Retzius neurons of the leech midbody ganglia respond in a complex manner to pressure pulses of acetylcholine (ACh) applied onto their soma with a fast depolarization followed by a slower hyperpolarization and an additional delayed long-lasting depolarization....

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Szczupak L, Edgar J, Peralta ML, et al. Long-lasting depolarization of leech neurons mediated by receptors with a nicotinic binding site. J Exp Biol. 1998;201:1895-906
Szczupak, L., Edgar, J., Peralta, M. L., & Kristan, W. B. (1998). Long-lasting depolarization of leech neurons mediated by receptors with a nicotinic binding site. The Journal of experimental biology, 2011895-906.
Szczupak, et al. "Long-lasting depolarization of leech neurons mediated by receptors with a nicotinic binding site." The Journal of experimental biology vol. 201 (1998): 1895-906.
Szczupak L, Edgar J, Peralta ML, Kristan WB. Long-lasting depolarization of leech neurons mediated by receptors with a nicotinic binding site. J Exp Biol. 1998 May 21;201:1895-906. PMID: 9600871.
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The effects of adrenaline and atropine on oxytocin-induced estrus in the goat.

Theriogenology

Cooke RG, Payne JH.
PMID: 16727077
Theriogenology. 1992 Apr;37(4):761-7. doi: 10.1016/0093-691x(92)90039-t.

Oxytocin-induced luteolysis in goats was associated with significant increases in peripheral plasma concentrations of 13,14-dihydro-15-keto-prostaglandin (PG) F(2alpha) (PGFM). This effect was not inhibited by concomitant administration of adrenaline (1 mg), although increases of PGFM were both delayed and diminished....

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Cooke RG, Payne JH. The effects of adrenaline and atropine on oxytocin-induced estrus in the goat. Theriogenology. 1992;37(4):761-7doi: 10.1016/0093-691x(92)90039-t.
Cooke, R. G., & Payne, J. H. (1992). The effects of adrenaline and atropine on oxytocin-induced estrus in the goat. Theriogenology, 37(4), 761-7. https://doi.org/10.1016/0093-691x(92)90039-t
Cooke, R G, and Payne, J H. "The effects of adrenaline and atropine on oxytocin-induced estrus in the goat." Theriogenology vol. 37,4 (1992): 761-7. doi: https://doi.org/10.1016/0093-691x(92)90039-t
Cooke RG, Payne JH. The effects of adrenaline and atropine on oxytocin-induced estrus in the goat. Theriogenology. 1992 Apr;37(4):761-7. doi: 10.1016/0093-691x(92)90039-t. PMID: 16727077.
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Erratum.

Science (New York, N.Y.)

[No authors listed]
PMID: 17745553
Science. 1978 Apr 21;200(4339):286. doi: 10.1126/science.200.4339.286-a.

The correct legend for the cover of the 31 March 1978 issue of Science is as follows: Hindfoot prints of a 6-hydroxydopamine-treated rat. Although typically akinetic when it is induced to walk by atropine, the rat's gait is characterized...

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Erratum. Science. 1978;200(4339):286doi: 10.1126/science.200.4339.286-a.
(1978). Erratum. Science (New York, N.Y.), 200(4339), 286. https://doi.org/10.1126/science.200.4339.286-a
"Erratum." Science (New York, N.Y.) vol. 200,4339 (1978): 286. doi: https://doi.org/10.1126/science.200.4339.286-a
Erratum. Science. 1978 Apr 21;200(4339):286. doi: 10.1126/science.200.4339.286-a. PMID: 17745553.
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Showing 37 to 48 of 1115 entries