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)

Data obtained suggest that preganglionic stimulation of the ciliary ganglion produces an increase of aqueous humor formation and of facility of outflow "C" through the following neurogenic pathway: (1) the preganglionic fibers synapse in the ciliary ganglion as evidenced by depression of the response with nicotine applied topically to the ganglion. (2) The impulse proceeds to the equivalent of an intraocular interneuron which can be blocked by low concentrations of atropine and has been previously identified as being an E-2 receptor site. (3) From the interneuron, activity is ultimately exerted without further synapse on alpha-adrenergic receptors through the release of norepinephrine from the neuronal terminals. The adrenergic mechanism of action is supported by the inhibition of the responses by phenoxybenzamine, bretylium, and guanethidine. Constriction of efferent ciliary process blood vessels by neuron-released norepinephrine seems to be the end effect responsible for the increased production of aqueous humor. The site of the end response to increase "C" is unclear.
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PMID:Ciliary ganglion stimulation. II. Neurogenic, intraocular pathway for excitatory effects on aqueous humor production and outflow. 113 43

N,N-Diethyl-2-(1-pyridyl)-ethylamine (E-2-P) has been shown previously to behave as a simple partial agonist at the histamine H1-receptor of guinea-pig ileum. When isolated longitudinal muscle strips from this preparation were tested with E-2-P before and after blockade with 2-haloalkylamines, it was found that these agents produced an irreversible shift to the right in the dose-response curve without significant depression of the maximum response even at very high antagonist concentrations. Under these circumstances the maximum response to the partial agonist may exceed the maximum response to histamine itself since the latter shows a much diminished maximum response at a very high concentrations of antagonist. These findings are not readily explicable in terms the usual "receptor-reserve' model of the histamine receptor system in ileum. A tentative explanation is provided, involving interaction with the antagonist at more than one site.
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PMID:Irreversible blockade of responses to a partial agonist acting at the histamine H1-receptor. 706 Jun 32

N,N-Diethyl-2-(1-pyridyl)ethylamine (E-2-P) produced 59 +/- 7% of the maximal response to histamine in guinea pig ileal longitudinal smooth muscle and antagonized the responses of this tissue to histamine. The estimated binding constant of E-2-P for the histamine receptor predicted a binding curve nearly coincident with the agonist concentration-response curve indicating no receptor reserve for this partial agonist. Diphenhydramine (30 nM) produced competitive antagonism of response to E-2-P (pKB = 8.3 +/- 0.13). Triprolidine (0.3 nM), a slower acting antihistamine, produced a depression of the maximal responses to E-2-P. This effect was analyzed in terms of a "hemi-equilibrium" hypothesis which approximates a pseudoirreversible antagonism of histamine receptors by triprolidine with respect to E-2-P. All data are consistent with the classification of E-2-P as a simple partial agonist for the histamine receptor of guinea pig ileum.
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PMID:N,N-Diethyl-2-(1-pyridyl)ethylamine, a partial agonist for the histamine receptor in guinea pig ileum. 721

The effect on mitochondrial outer membrane of 4-hydroxychalcone (1), the cyclic chalcone analogues E-2-(4'-hydroxybenzylidene)-1-indanone (2a) and E-2-(4'-hydroxybenzylidene)-1-tetralone (2b), the dihydrochalcones phloretin (3a) and phloridzin (3b), the flavanones naringenin (4a) and naringin (4b), and the flavonol quercetin (5) was investigated by fluorescence spectroscopy. Excitation and emission fluorescence spectra of each flavonoid and synthetic analogue were recorded in respiration medium containing 1 mM succinate. Initial interaction of the compounds with the outer mitochondrial membrane was investigated by recording their fluorescence polarization in the presence of rat liver mitochondria. Most of the compounds displayed an elevated fluorescence polarization on mixing with mitochondria at the zero time point. During the investigated 20 min period the initial fluorescence polarization values remained constant (1, 2a), or a gradual depression of the measured polarization values could be observed (2b, 3a, 4b, 5). In the case of naringenin (4a), however, similar to the previously investigated seven-membered cyclic chalcone analogue E-2-(4 -methoxybenzylidene)-1-benzosuberone, a slight, continuous increase of fluorescence polarization could be detected during the 20 min experiment. Phloridzin (3b) showed an increased fluorescence polarization in first 10 min, which was slightly depressed by the 20 min time point.
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PMID:Comparison of the effects of selected chalcones, dihydrochalcones and some cyclic flavonoids on mitochondrial outer membrane determined by fluorescence spectroscopy. 1681 66

There is relatively little research on the Personality Assessment Inventory (PAI) with mild traumatic brain injury (MTBI) populations. There is also little research on how compensation-seeking status affects personality assessment results in MTBI patients. The current study examined the PAI scales and subscales in two MTBI groups, one composed of compensation-seeking MTBI patients and the other consisting of non-compensation-seeking MTBI patients. Results indicated significant differences on several scales and subscales between the two MTBI groups, with the compensation-seeking MTBI patients having significantly higher elevations on scales related to somatic preoccupation (Somatic Complaint Scale, SOM), emotional distress (Anxiety Scale, ANX; Anxiety Related Disorders Scale, ARD; Depression Scale, DEP), and the Negative Impression Management, NIM, validity scale. All the SOM subscales and the Anxiety Cognitive (ANX-C) and ANX Affective, ANX-A, subscales were also elevated in the compensation-seeking group. Results indicated that several scales on the PAI were sensitive to group differences in compensation-seeking status in MTBI patients.
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PMID:Differential response patterns on the Personality Assessment Inventory (PAI) in compensation-seeking and non-compensation-seeking mild traumatic brain injury patients. 2213 11

The Coronavirus (2019-Cov-2) infection Covid-19 is highly contagious caused by single stranded RNA virus (+ssRNA) with nucleocapsid and spreading widely all across the world and responsible for more than 3.6 million morbidity and 0.25 million mortality No specific treatment is available till date. The clinical symptoms are mainly upper respiratory leading to diffuse viral pneumonia and multiple organ failure involving. Kidney, Liver and Heart along with coagulopathies. During 2004 (SARS-CoV) pandemic role of nitric oxide in its management is well demonstrated. Nitric Oxide (NO) reversed pulmonary hypertension. Improved severe hypoxia and shortened the stay in ICU and ventilatory support. Nitric Oxide increased the survival rate. The genetic composition of Corona Virus (SARS-CoV) is almost similar to Covid-19, thus indicates good chances of effectiveness or enhancement in results by Nitric Oxide along with other modes in treatment of Covid-19. It has been proved by studies by serendipity humming increases NO Expression dramatically.It is estimated that humming increases the endogenous generation of nitric oxide level by 15-fold. Hypoxia in ARD Syndrome leads to blood coagulation by depression of body defence anticoagulatory and fibrolytic properties along with metabolic acidosis. If we go into hypoxic hypercapnic state no hyper coagulation takes place. Hence Bhramari by enhancing the expression of Nitric Oxide and increased Carbon dioxide by extended exhalation and alkaline pH prevents coagulopathies and morbidity due to Covid-19.
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PMID:Modified Bhramari Pranayama in Covid 19 Infection. 3271 37