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

Acute spinal and curarized cats can generate "fictive locomotor activity" after an i.v. injection of Nialamid followed by 4-AP and L-DOPA. The efferent burst activity to flexors and extensors can be recorded in peripheral nerve filaments. Ramp-formed movements were applied in the hip at constant angular velocity in different phases of the spontaneous efferent burst activity. The cycle duration was markedly influenced. A flexion or an extension ramp applied in the early part of the "step-cycle" (during flexor activity) will prolong the cycle duration, but in the later part of the cycle instead a marked shortening effect will occur. The transition from a prolongation to a shortening is very steep for the extensive-ramps, with a subsequent gradual increase from a shortening to a lengthening of the cycle. This type of phase response curve expresses a potent peripheral modulatory effect on the central pattern generator. A ramp movement (flexion or extension) applied in the beginning of the flexor burst will reinforce the flexor activity. In the end of the flexor burst instead there is a directional sensitivity with positive feedback, resulting in an excitation of the flexor activity for flexion ramps, but a depression of the flexor activity for extension-ramps. Extension-ramps also show a position dependent effect which enhances the response in the flexors for more extended hip positions.
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PMID:Peripheral control of the cat's step cycle. I. Phase dependent effects of ramp-movements of the hip during "fictive locomotion". 731 42

Random copolymers of adenylic acid and 2-aminoadenylic acid form both double and triple helices with poly(uridylic acid) [poly(U)]. Transition temperatures of two-stranded helices increase with 2NH2A content, exhibiting a slight positive departure from linearity and indicating that the contribution to helix stability arising from introduction of the 2-amino group does not significantly depend upon base sequence. We have shown previously that poly(2NH2A) . poly(U) does not undergo a disproportionation reaction (2 leads to 3 transition). Extrapolation from melting curves of 1:1 complexes between A,2NH2A copolymers and poly(U) indicates a Tm for the 2 leads to 3 transition of poly(2NH2A) . poly(U) which is too high to be observable under normal conditions. Addition of an organic solvent (50% ethylene glycol), however, lowers Tm by promoting unstacking of single-stranded poly(2NH2A) sufficiently to permit observation of the disproportionation of poly(2NH2A) . poly(U) for the first time. Transition breadths of 1:1 complexes of A,2NH2A copolymers with poly(U) are greater than those of either of the homopolymer complexes in the middle range of composition (67 and 48% A) but not at 25% A. These results are consistent with previous calculations on the effect of heterogeneity in base-pair stability on DNA transition breadths. In the poly(A), poly(U) system, Et4N+ counterion reduces the Tm of the double and triple helices by 26 and 41 degrees C, respectively. The larger depression in the latter case arises from the higher charge density of the triple helix and less effective counterion screening by Et4N+. In the poly(2NH2A), poly(U) system Tm,2 leads to 1 is reduced by 24 degrees C, but extrapolation of the copolymer results indicates a reduction of approximately 100 degrees C for Tm,3 leads to 2, accounting for previous failure to observe a triple helix in this system. CD spectra of A,2NH2A copolymers suggest that much of the spectral region can be regarded as a contribution of the CD spectra of the parent polymers poly(A) and poly(2NH2A) but that the region from 255 to 275 nm requires that contributions made by longer range interactions be taken into account.
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PMID:Copolymers of adenylic and 2-aminoadenylic acids. Effect of progressive changes in hydrogen bonding and stacking on interaction with poly(uridylic acid). 738 83

Production of oxygen-free radicals has been proposed as one pathophysiologic mechanism for postburn cardiac contractile dysfunction in adults. To examine this hypothesis in young subjects, we studied the cardiac effects of polyethylene glycol-superoxide dismutase (PEG-SOD) and PEG-catalase (PEG-CAT), each given as 20 U/g of body weight with fluid resuscitation (Parkland formula), after a third-degree burn constituting 33% of the total body surface area in young (6- to 7-day old) guinea pigs (group 3, n = 12). Fluid-treated burns without scavenger therapy (group 2, n = 15) and sham burn controls (group 1, n = 15) were included. Animals were killed 24 hours postburn, and hearts were studied in vitro (Langendorff). Compared with sham burn controls, fluid-treated burns (group 2) had significant cardiac dysfunction as indicated by a lower peak systolic left ventricular (LV) pressure (LVP: 67 +/- 2 vs. 57 +/- 4 mm Hg, p = 0.01, mean +/- SEM), maximal rate of LV pressure development (+dP/dt max: 1169 +/- 45 vs. 988 +/- 45 mm Hg/second, p = 0.01), and fall (-dP/dt max: 1109 +/- 45 vs. 919 +/- 49 mm Hg/second, p = 0.01). In addition, LV function curves calculated for group 2 were shifted downward and to the right of those calculated for sham burn controls in the direction of contractile depression, p = 0.01. PEG-SOD/PEG-CAT treatment in burns did not significantly improve LVP (60 +/- 5 mm Hg), but scavenger therapy improved +/-dP/dt max values (1112 +/- 74 and 988 +/- 98 mm Hg/second, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of toxic oxygen metabolites in a young model of thermal injury. 747 25

The authors describe empirical corrections to ideally dilute expressions for freezing point depression of aqueous solutions to arrive at new expressions accurate up to three molal concentration. The method assumes non-ideality is due primarily to solute/solvent interactions such that the correct free water mass Mwc is the mass of water in solution Mw minus I.M(s) where M(s) is the mass of solute and I an empirical solute/solvent interaction coefficient. The interaction coefficient is easily derived from the constant in the linear regression fit to the experimental plot of Mw/M(s) as a function of 1/delta T (inverse freezing point depression). The I-value, when substituted into the new thermodynamic expressions derived from the assumption of equivalent activity of water in solution and ice, provides accurate predictions of freezing point depression (+/- 0.05 degrees C) up to 2.5 molal concentration for all the test molecules evaluated; glucose, sucrose, glycerol and ethylene glycol. The concentration limit is the approximate monolayer water coverage limit for the solutes which suggests that direct solute/solute interactions are negligible below this limit. This is contrary to the view of many authors due to the common practice of including hydration forces (a soft potential added to the hard core atomic potential) in the interaction potential between solute particles. When this is recognized the two viewpoints are in fundamental agreement.
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PMID:Correction for solute/solvent interaction extends accurate freezing point depression theory to high concentration range. 769

Monocrotophos is a water-soluble organophosphate insecticide with high oral and moderate dermal toxicity. The toxicologically relevant mode of action is the inhibition of ChE activities. The toxicity of organophosphate metabolites of monocrotophos is comparable with the parent compound. Glycol conjugation in plant metabolism decreased the acute toxicity significantly. Dephosphorylated metabolites showed no demonstrable acute toxicity. Repeated exposure to the compound leads to initial cumulation of the single-dose effects. At moderate dose levels, the adverse effects are counteracted by an increase of tolerance through adaptation. A study in humans demonstrated no relevant ChE depression over a 30-d period at daily dose levels of up to 0.006 mg/kg. Lifetime chronic feeding studies in rodents again indicated ChE inhibition as the only specific effect. Body weight reduction was limited to high doses. No gross or microscopic specific lesions were demonstrable; especially, there was no evidence of oncogenic effects. Genotoxicity was evident in vitro, whereas comprehensive assessment of the in vivo tests indicates no toxicologically relevant mutagenic potential in mammals. This conclusion is supported by the absence of oncogenic effects in chronic feeding trials. Findings in reproduction studies were limited to secondary fetal reactions that were triggered by maternal toxicity. Acute and repeated administration studies in hens revealed no delayed (degenerative) neurotoxic potential. Monocrotophos showed no significant potentiation with 24 other ChE inhibitors. Poisoning signs after heavy doses were controlled by therapeutic doses of atropine, preferably in combination with an oxime.
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PMID:Toxicology of monocrotophos. 780 17

4-Methylpyrazole (4-MP), an alcohol dehydrogenase inhibitor, was administered to dogs to treat ethylene glycol (EG) intoxication. Eleven dogs were given 10.6 g of EG/kg of body weight; 5 dogs were treated with 4-MP 5 hours after EG ingestion and 6 dogs were treated with 4-MP 8 hours after EG ingestion. 4-Methylpyrazole was administered IV as a 50-mg/ml [corrected] solution in 50% polyethylene glycol: initial dose, 20 mg/kg; at 12 hours after initial dose, 15 mg/kg; at 24 hours after initial dose, 10 mg/kg; and at 30 hours after initial dose, 5 mg/kg. Physical, biochemical, hematologic, blood gas, serum and urine EG concentrations, and urinalysis findings were evaluated at 0, 1, 3, 6, 9, 12, 24, 48, 72 hours, and at 1 week and 2 weeks after EG ingestion. Dogs of both groups developed clinicopathologic signs associated with EG intoxication, including CNS depression, hyperosmolality, high anion gap metabolic acidosis, polydipsia, polyuria, calcium oxalate monohydrate and dihydrate crystalluria, and isosthenuria. Fractional excretion of sodium was increased in all dogs between 1 and 9 hours after EG ingestion, but remained increased beyond 24 hours only in the 2 dogs treated at 8 hours after EG ingestion that developed acute renal failure. All dogs treated 5 hours after EG ingestion recovered without morphologic, biochemical, or clinical evidence of renal impairment. Of the 6 dogs treated 8 hours after EG ingestion, 2 developed acute renal failure. One of the dogs treated 8 hours after EG ingestion remained isosthenuric for 2 months, but did not manifest any other signs of renal impairment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Efficacy of 4-methylpyrazole for treatment of ethylene glycol intoxication in dogs. 788 24

The intravenous anesthestic thiopental has been previously shown to increase the incidence of ventricular arrhythmias, particularly when combined with epinephrine and halothane. Recent work based on microelectrode and tension measurements has indicated that thiopental may diminish membrane K+ permeability. Utilizing the whole-cell patch-clamp technique, we investigated the effect of thiopental on the current associated with the resting membrane conductance, the anomalous or inward rectifying K+ current (IK1). External application of 30 microM thiopental to frog atrial myocytes resulted in a 56 +/- 2% (mean +/- S.E.M.; n = 12 cells) reduction in the magnitude of IK1 elicited by a hyperpolarization to -110 mV. The outward current component through IK1 channels, evoked by depolarizing voltages above the resting potential, was decreased to same extent. The effect of thiopental on IK1 was concentration-dependent and the time courses of onset and recovery were rapid (tau = 10-14 sec). Ramp command potentials from -120 to +60 mV at a rate of 20 mV/sec revealed that 30 microM thiopental also depressed the delayed outward K+ current by 25 +/- 4% (n = 4). Examination of other barbiturates revealed that the potency in the suppression of IK1 was related to the octanol/water partition coefficient, suggesting a lipophilic site of action. Utilizing guinea pig ventricular myocytes, we observed a similar level of IK1 depression with thiopental, however the rates of onset and recovery were considerably slower than with frog atrial myocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Barbiturate anesthetics depress the resting K+ conductance of myocardium. 847 18

A new highly accurate curve-fitting technique for looking at freezing-point depression data was proposed by Fullerton et al. (Biochem. Cell Biol., in press). The method involve plotting mass solvent to mass solute ratio (Mw/M(s)) vs. 1/delta T (i.e. the inverse change in freezing point). A measured molecular weight and a solute/solvent interaction parameter (called I value) are inferred from the resultant linear plot. The accuracy of the molecular weight method was first demonstrated with the monomers of ethylene glycol, glycerol, propanol, mannitol, glucose and sucrose to show a mean molecular weight error of 0.02% with root mean square (RMS) error 0.9%. The RMS error (0.9%) is our best estimate of the molecular weight measurement accuracy for the method applied to a monomer. This error is consistent with the experimental precision (approximately 1%) which implies no systematic error. Non-ideality is described with a single constant, I. Polyethylene glycol (PEG) polymers of increasing length (vendor designation 200 to 10,000 Da) were analyzed to show monotonically increasing non-ideality (I values of 0.12 to 3.67) with increasing molecular weight. The measured molecular weights agreed with the end-point titration value for the three smallest polymers (where the number of polymeric units was less than or equal to 7). The method underestimates the vendor molecular weights for longer polymers. This disagreement is assigned to segmental motion (internal entropy) of longer, more flexible, PEG molecules.
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PMID:Solute/solvent interaction corrections account for non-ideal freezing point depression. 848 91

The effect of adding cottonseed hulls to casein- and cottonseed-kernel-based diets on the apparent and true ileal digestibility of N and amino acids, and the proportion of this effect accounted for by condensed tannin (CT), were determined using the growing rat. Sixty rats were allocated randomly to ten semipurified diets, containing either casein (four diets) or purified unheated solvent-extracted cottonseed kernel (six diets) as the sole protein source, with Cr2O3 added as an indigestible marker. Two of the casein diets contained no hulls whilst the remaining two diets contained 70 g cottonseed hulls/kg. Two of the cottonseed-kernel-based diets contained no hulls, with two containing 23 g hulls/kg and the remaining two containing 46 g hulls/kg. For each pair of diets, PEG was either included or excluded. The effect of CT was quantified by comparing control rats (-PEG; CT acting) with PEG-supplemented rats (+PEG; CT inactivated) at each level of dietary hulls. The rats were given their respective experimental diets for 14 d. Each rat was given the food ad libitum for 10 min hourly from 08.00 to 18.00 hours. On day 14, samples of digesta were collected at death from the terminal 150 mm of ileum at 7 h from the first meal. Apparent and true ileal digestibilities were calculated for DM, N and the individual amino acids. The principal finding was that the inclusion of hulls depressed the apparent and true ileal digestibilities of N and amino acids, but with the response differing between diets. With the casein-based diet the mean apparent and true ileal amino acid digestibilities were significantly depressed from 0.89 and 0.96 to 0.85 and 0.92 respectively, by the inclusion of 70 g hulls/kg in the diet, and addition of PEG then restored these to 0.89 and 0.95. All of the depression could be explained by the CT content of the hulls. However, with the cottonseed-kernel-based diet the responses fell into three categories. The apparent and true ileal digestibilities of the essential amino acids cystine and methionine were not affected by hull addition, ileal digestibilities of leucine, isoleucine, lysine, threonine and valine were markedly depressed by hull addition with approximately 50% of the depression being explained by CT, whilst the ileal digestibilities of histidine, arginine and phenylalanine were depressed by hull addition but little or none of this effect could be explained by CT. Thus the effect of hulls on protein digestion clearly differed with source of protein. With the cottonseed-kernel-based diet it seems that components of the hulls other than CT also depressed the apparent and true ileal digestibilities of N and amino acids. The identity of these components is unknown.
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PMID:The effect of cottonseed condensed tannins on the ileal digestibility of amino acids in casein and cottonseed kernel. 869 96

1. The black widow spider venom component, alpha-latrotoxin (alpha-LTx) (< 0.5 nM), increased the frequency of miniature excitatory postsynaptic currents (mEPSCs) in hippocampal CA3 pyramidal cells 14-fold, without changing their amplitude. 2. This action of alpha-LTx was not affected by application of Ca(2+)-free/ethylene glycol-bis(b-aminoethyl ether)-N,N,N',N'-tetraacetic acid-containing saline, 100 microM Cd2+, or 50 microM Gd3+. The increase in mEPSC frequency was thus not due to an influx of Ca2+ into the axon terminal via voltage-dependent Ca2+ channels or alpha-LTx-induced pores. 3. alpha-LTx did not increase spontaneous release when synaptic transmission had been impaired by botulinum toxin/F. 4. alpha-LTx reduced the amplitude of EPSCs, elicited with stimulation of mossy fibers, without affecting paired-pulse facilitation. 5. The Ca2+ ionophore ionomycin (2-2.5 microM) also enhanced the frequency of mEPSCs, but unlike alpha-LTx, potentiated evoked EPSCs and reduced paired-pulse facilitation. Application of N-methyl-D-aspartate elicited a high frequency of Ca(2+)-dependent, tetrodotoxin-sensitive spontaneous EPSCs, but did not affect evoked EPSC amplitude. Agents that stimulate vesicular release by increasing presynaptic Ca2+ influx thus do not mimic the alpha-LTx-induced depression of evoked EPSCs. 6. We conclude that entry of Ca2+ into presynaptic axon terminals is not responsible for the effects of low concentrations of alpha-LTx on either spontaneous or evoked transmitter release in the hippocampus. 7. Potential presynaptic mechanisms that could mediate the opposing actions of alpha-LTx on spontaneous and evoked transmitter release in the hippocampus (i.e., alpha-LTx-induced ionic pores, depletion of synaptic vesicles, actions on exocytotic proteins) are discussed.
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PMID:Calcium-independent actions of alpha-latrotoxin on spontaneous and evoked synaptic transmission in the hippocampus. 893 Feb 62


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