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Biomedical subjects

J G Collins

Publications and source records attributed to J G Collins.

At least 73 records · Page 4Linked to original sources
PubMed1993

Prevalence of selected chronic conditions: United States, 1986-88.

Estimates of the prevalence of selected chronic conditions are presented by biological system involved, sex, age, race, family income, geographic region, and place of residence. The percent of conditions causing limitation of activity, the percent of conditions for which a physician was consulted, and the number of restricted-activity days and bed-disability days resulting from the conditions are also included.

Activities of Daily Living↗
PubMed1991

Zn(2+)-induced deprotonation of a peptide nitrogen in angiotensin I.

The interaction of Zn2+ with angiotensin I, a decapeptide containing two histidyl residues, has been studied by 1H-NMR spectroscopy in both water and dimethylsulfoxide. When Zn2+ is added to the peptide in dimethylsulfoxide, binding occurs by coordination of the imidazole rings of both histidines to the metal-ion, enabling the deprotonation of the Phe peptide nitrogen.

Amino Acid Sequence↗
PubMed1991

Delta receptor involvement in morphine suppression of noxiously evoked activity of spinal WDR neurons in cats.

Morphine has been considered to be primarily a mu opiate receptor agonist. The present study was designed to determine if opiate receptor subtypes in addition to mu contribute to morphine analgesia at the level of the spinal cord. Extracellular activity of single wide dynamic range (WDR) neurons in the feline lumbar spinal cord were studied. Intrathecal administration of DAGO (selective mu agonist) or DPDPE (selective delta agonist) suppressed the noxiously (51 degrees C radiant heat) evoked activity of WDR neurons. Pretreatment with spinal beta-FNA (selective mu antagonist) antagonized the suppressive effects of spinal DAGO, but not that of DPDPE. Two doses of spinal morphine (200 and 400 micrograms) suppressed the noxiously evoked activity of WDR neurons confirming our previous report. Following beta-FNA pretreatment, the suppressive effects of morphine were reduced, however, when ICI 174,864 (selective delta antagonist) was co-administered with morphine on the spinal cord of the animals pretreated by beta-FNA, there was an even greater reduction in the neuronal suppression by morphine. Intravenous ICI 174,864 also reversed the suppressive effects of morphine in beta-FNA pretreated animals. beta-FNA antagonism of spinal morphine is evidence of the well-known mu receptor-mediating antinociception. However, antagonism by ICI 174,864 of morphine suppression in beta-FNA-pretreated animals demonstrates that morphine is capable of suppressing noxiously evoked activity of WDR neurons as a result of an interaction with delta receptors in addition to mu receptors at the level of spinal cord.

Analgesia↗
PubMed1991

Interaction between opiate subtype and alpha-2 adrenergic agonists in suppression of noxiously evoked activity of WDR neurons in the spinal dorsal horn.

Several studies have demonstrated synergistic antinociception following low-dose administration of morphine and alpha-2 adrenergic agonists at the spinal level. This study was carried out in order to identify the opiate subtypes that are likely to be involved in such synergistic suppression of noxiously evoked activity of wide-dynamic-range (WDR) neurons in the dorsal horn of the spinal cord. We also examined the effect of opiate antagonists and alpha-2 adrenergic antagonists on the suppression produced by opiate or alpha-2 adrenergic agonists. Extracellular activity of single WDR neurons in the spinal dorsal horn, which was evoked by a radiant heat stimulus (51 degrees C), was recorded in decerebrate, spinally transected cats. Agonists were administered spinally and antagonists intravenously. In the synergism study, ineffective doses of the moderately selective mu agonist morphine (25 micrograms), the delta agonist DADL (20 micrograms), and the selective delta agonist DPDPE (30 micrograms), when combined with an ineffective dose of the alpha-2 adrenergic agonist clonidine (5 micrograms) produced significant synergistic suppression of noxiously evoked WDR neuronal activity. However, the ineffective or slightly effective dose of the selective mu agonist DAGO (1 or 1.5 micrograms, respectively) did not show any synergistic action with clonidine. Furthermore, the synergism between morphine and clonidine was reversed by the selective delta antagonist ICI 174,864. We interpret these results to indicate that opiates interact at spinal delta receptors to produce a synergistic suppression of evoked WDR neuronal activity in the presence of spinal clonidine. An alternative explanation is that ICI 174,864 may interact in some way with alpha-adrenergic systems.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1991

Naloxone-sensitive, pregnancy-induced changes in behavioral responses to colorectal distention: pregnancy-induced analgesia to visceral stimulation.

This study examined the feasibility of using colorectal distention as a noxious visceral stimulus in rat pregnancy-induced analgesia studies as well as the influence of naloxone on the pregnancy-induced changes in the behavioral response to a noxious visceral stimulus. In the first part of the study, we compared the effects of pregnancy on several forms of noxious stimulation (colorectal distention, hypertonic saline induced writhing, tail flick, and hot plate). After determination of prepregnant baseline values, one group of rats (n = 35) was mated and retested on days 7 and 21 of gestation and 1, 3, 5, 7, and 14 days after parturition. After baseline determinations on day 21 and postpartum day 1, the animals received a subcutaneous injection of naloxone 1.0 mg/kg and were retested. A nonpregnant control group of animals (n = 7) was tested in the same manner. On day 21 of gestation and postpartum days 1 and 3, significant changes (higher threshold or longer latency to response) were observed after all but the writhing test. High-dose naloxone (1.0 mg/kg) significantly reduced the increases observed on day 21 and post-partum day 1. Nonpregnant rats demonstrated no significant change on any test day. The second part of the study evaluated a possible influence of low-dose naloxone on pregnancy-induced analgesia to visceral stimulation (colorectal distention) in another group of pregnant rats (n = 44). The significant increase in threshold on day 21 of gestation was not changed by intravenous (i.v.) naloxone 1.0, 2.3, or 3.0 micrograms/kg, whereas 5.0 and 20.0 micrograms/kg naloxone significantly decreased the observed pregnancy-induced analgesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia, Obstetrical↗
PubMed1991

Low-dose clonidine enhances pregnancy-induced analgesia to visceral but not somatic stimuli in rats.

This is one of a series of experiments designed to examine the possible pharmacologic basis for analgesia normally associated with pregnancy. The antinociceptive effects of low-dose (0.1 mg/kg) subcutaneous clonidine on analgesia associated with pregnancy were evaluated in rats. Colorectal distention thresholds and tail-flick latencies were determined in timed pregnant rats (n = 27) before mating, on days 7 and 21 of gestation, and on postpartum day 7. Immediately after baseline testing on each of those days, animals received 0.1 mg/kg clonidine subcutaneously and were retested 30 min later. On day 21 of gestation, 20 micrograms/kg naloxone (n = 9) and 0.2 mg/kg yohimbine (n = 5) were intravenously administered after clonidine testing, and animals were retested 15 min later. In the absence of clonidine, pregnant animals demonstrated a statistically significant increase in their tolerance of colorectal distention pressures and longer latencies to tail-flick withdrawal on day 21 of gestation. Clonidine produced a further significant increase in distention thresholds on day 21 of gestation but did not change these thresholds on any other day, nor did it change tail-flick latencies. Naloxone and yohimbine reversed the effect of clonidine on the distention thresholds on day 21. Systemic clonidine, at a dose lower than that required to produce antinociception in nonpregnant rats, enhanced pregnancy-induced analgesia to visceral stimulation late in pregnancy, an effect that was reversed by naloxone and yohimbine. These results suggest a synergistic antinociceptive effect of clonidine due to an interaction with an endogenous opiate system that is only activated late in pregnancy.

Analgesia, Obstetrical↗
PubMed1991

[Effects of ketamine on behavioral responses to somatic and visceral stimuli in rats].

The responses to colorectal distension as a visceral stimulus were observed and tail-flick test was performed in rats, after intraperitoneal administration of ketamine 30 mg.kg-1 (n = 6) or 100 mg.kg-1 (n = 5). After determining control colorectal distension and tail-flick values, both procedures were repeated every 10 minutes for one hour in both groups. The control thresholds for colorectal distension and tail-flick latencies were 20.8 +/- 1.0 mmHg and 4.5 +/- 0.3 sec (mean +/- SD), respectively in ketamine 30 mg.kg-1 group. They were 21.2 +/- 1.1 mmHg and 4.7 +/- 0.4 sec in ketamine 100 mg.kg-1 group. These baseline threshold and latency values in the two groups were not significantly different. Ten minutes after ketamine administration, the colorectal distension thresholds and tail-flick latencies were 43.7 +/- 7.2 mmHg and 6.4 +/- 0.9 sec, respectively in ketamine 30 mg.kg-1 group. They were 53.3 +/- 14.8 mmHg and 7.2 +/- 0.8 sec, respectively in ketamine 100 mg.kg-1 group. These values were significantly greater than the preketamine control values in both groups. The present study demonstrates that ketamine exerts apparent analgesic effects against both visceral and somatic stimuli. These results led us to consider that ketamine may be clinically useful to control visceral pain.

Animals↗
PubMed1991

Monitoring anthracycline binding to nucleotides by two dimensional cosy NMR experiments.

The nucleotide binding ability of the novel anthracycline drug, 3-fluoro-4-demethoxydaunomycin, has been studied by two dimensional 1H NMR correlated spectroscopy (COSY). In the COSY spectrum of the nucleotide mini-helix d(CTGCAG)2 cross-peaks are observed from the spin-coupled H6 and H5 protons of the cytidine bases. Additional cytidine H6/H5 cross-peaks are observed in the COSY spectrum of the anthracycline-d(CTGCAG)2 complex. These additional cytidine cross-peaks enable the identification of the anthracycline binding sites and the determination of the relative kinetic stability of the bound drug at each binding site.

Binding Sites↗
PubMed1991

Impairments due to injuries: United States, 1985-87.

Estimates of the number of selected impairments due to injuries, by type of impairment, are presented by age, cross-tabulated by sex, race, geographic region, place of residence, family income, education of responsible adult family member, living arrangement, marital status, respondent-assessed health status, and employment status. Selected impairments due to injuries are also shown by class and place of accident, resulting limitation of activity, and disability days.

Accidents↗
PubMed1991

[Comparison of the effect of propofol and that of pentobarbital on behavioral responses to somatic and visceral stimuli in rats].

The behavioral responses to tail-flick and colorectal distension after intraperitoneal administration of either small or large dose of propofol as well as of pentobarbital were studied in rats. Immediately after baseline testing, animals were randomly divided into four groups; propofol groups of 50 mg.kg-1 (n = 4) or 100 mg.kg-1 (n = 4) and pentobarbital groups of 10 mg.kg-1 (n = 4) or 20 mg.kg-1 (n = 4). Both tests were repeated every 10 minutes for 1 hour in each group. There were no changes in the thresholds of colorectal distension and tail-flick latencies in those animals receiving small doses of propofol and pentobarbital. The thresholds for colorectal distension following administration of large doses of propofol and pentobarbital had greatly increased at 10 minutes and this increase persisted for about 30 minutes although it declined gradually. In contrast, the state of high sensitivity to tail-flick test was seen in the large dose groups of both drugs. It is concluded that there are no pharmacological differences between propofol and pentobarbital in behavioral responses to somatic and visceral stimuli in rats.

Animals↗
PubMed1990

Plasticity of some spinal dorsal horn neurons as revealed by pentobarbital-induced disinhibition.

Extracellular activity was recorded from single spinal dorsal horn neurons in physiologically intact, awake, drug-free cats before and after the intravenous administration of 20 mg/kg pentobarbital (Pb). Pb produced a series of changes in response properties that reflect a significant moment-to-moment plasticity of some spinal dorsal horn neurons. Pb administration unmasked the ability of some low-threshold (LT) neurons to respond to noxious mechanical or thermal stimuli resulting in their being reclassified as wide dynamic range (WDR) neurons. Pb also appeared to unmask an afterdischarge in some neurons following noxious mechanical stimulation. In addition, some neurons appeared to be better able to signal changes in the intensity of mechanical stimulation after Pb. Neuronal receptive fields for low threshold stimulation were reduced in many instances but enlargement was also observed. The responses of some neurons to peripheral stimulation were unchanged by Pb. We hypothesize that the relatively low doses of Pb used in the study reduced tonic inhibition of some spinal dorsal neurons although the observed effects could have been produced by excitation.

Animals↗
PubMed1990

A 19F-NMR study of 3-fluoro-4-demethoxydaunomycin intercalation complexes with the hexanucleotide d(CTGCAG)2.

Equilibrium systems containing intercalation complexes formed between the novel anthracycline drug, 3-fluoro-4-demethoxydaunomycin (3FD), and the hexanucleotide duplex d(CTGCAG)2 have been studied by 19F-NMR spectroscopy. Solutions containing a 1:1 molar ratio of 3FD/d(CTGCAG)2 gave four 19F signals which have been assigned to each of four possible intercalation isomers for the 1:1 3FD.d(CTGCAG)2 complex, which we denote by [d(CTGCAG)2][3FD]; these were where 3FD bound between the 5'-CT-3', 5'-TG-3', 5'-GC-3' or 5'-CA-3' base sequences, with the drug sugar moiety lying in the minor groove and pointed in the 3' direction in each case. Changes in temperature and NaCl concentration affecting the equilibrium distribution of these isomers were studied and indicated that no overriding binding site preference prevailed under standard biochemical conditions. Formation of some of the 2:1 3FD.d(CTGCAG)2 complex occurred when a solution of [d(CTGCAG)2][3FD] was exposed to excess 3FD; however, this complex was unstable to gel filtration and no co-operative binding of the second 3FD molecule was observed.

Base Sequence↗
PubMed1990

NMR identification of a partial helical conformation for bombesin in solution.

The conformation of bombesin in trifluoroethanol/water mixtures has been studied using 1H-NMR spectroscopy. By a combination of two-dimensional 1H-NMR techniques and measurement of vicinal NH-alpha-CH spin-spin coupling constants, the secondary structure of the molecule has been determined. Bombesin adopts a helical structure in the region from Asn-6 to Met-14 with the remaining N-terminal portion existing as a more extended structure. The structure is very similar to that proposed from Fourier-transform infrared spectroscopic measurements for bombesin inserted into lipid bilayers [D. Erne & R. Schwyzer (1987) Biochemistry 26, 6316-6319]. The absence of a hydrogen bond between the sidechains of Trp-8 and His-12 is discussed in terms of the ionization state of His-12. Stabilisation of the helix results when His-12 is in the ionized state.

Bombesin↗
PubMed1990

Tonic 5-HT modulation of spinal dorsal horn neuron activity evoked by both noxious and non-noxious stimuli: a source of neuronal plasticity.

The influence of tonic serotonergic modulation on the responses of spinal dorsal horn neurons to natural peripheral stimulation was examined in physiologically intact, awake, drug-free cats. Systemically administered methysergide (maximum cumulative dose 2 mg/kg) caused significant changes in responses of some dorsal horn neurons to both mildly noxious and non-noxious stimulation. Individual changes provide evidence, in this model, for tonic 5-HT modulation of many aspects of sensory transmission at the level of the spinal cord. Taken together, the changes demonstrate the significant degree of plasticity that exists for some spinal dorsal horn neurons. It is clear that the plasticity of some spinal dorsal horn neurons allows for a much broader response profile than would be apparent under the restricted circumstances of a normal neurophysiologic study. Removal of tonic inhibition on responses to noxious stimuli may be an aspect of neuronal plasticity that functions to provide an immediate change in the way that the nervous system responds to a noxious stimulus.

Action Potentials↗