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Biomedical subjects

J G Collins

Publications and source records attributed to J G Collins.

At least 37 records · Page 2Linked to original sources
PubMed1997

In vitro attachment of osteoblast-like cells to osteoceramic materials.

OBJECTIVE: The objective of this work was to examine osteoblast-like cell attachment and morphology in vitro to osteoceramic materials with three different surface morphologies. METHODS: Osteoceramic composite disks were fabricated from tricalcium phosphate and magnesium-aluminate spinel (MgAl2O4) in a 50 vol% ratio. The disks were prepared with three different surface morphologies, including as-fired (irregular), etched (rough), or polished through 1 mm diamond paste (smooth). Osteoblast-like cell cultures were plated onto the prepared disks for 2 h, and the number of attached cells was determined. ANOVA and Student Newman-Kuels tests were used to test for significant differences in cell attachment (p < 0.05). SEM was used to visually evaluate the nature of the cellular adaptation on the osteoceramic surfaces. RESULTS: Some additional surface roughening resulted from the interaction between the osteoceramic disks and the biological culture media during the attachment assay. A statistically larger number of cells was found to be attached to the etched osteoceramic surfaces compared to the as-fired and polished osteoceramic surfaces or the tissue culture plastic control. Cellular adaptation was extensive on all three osteoceramic surfaces at 2 h. SIGNIFICANCE: These results are consistent with previous in vivo work and continue to support the hypothesis that osteoceramic materials have potential for implants and bone substitute materials.

Aluminum Compounds↗
PubMed1997

Monocytic TNF alpha secretion patterns in IDDM patients with periodontal diseases.

The aim of the present study was to identify whether monocytic TNF alpha secretion patterns could serve as a potential phenotypic discriminator for periodontal disease susceptibility within insulin-dependent diabetes mellitus (IDDM) patients. In 32 IDDM individuals the lipopolysaccharide (LPS) stimulated monocytic TNF alpha secretion dose-response characteristics were analyzed and related to two different periodontal status categories. Diabetics were divided into group A (gingivitis or mild periodontal disease) and group B (moderate to severe periodontal disease). In addition, 17 non-diabetic individuals with various degrees of periodontal disease served as control patients. Diabetics as a group had a significantly higher monocytic TNF alpha production in response to increasing Porphyromonas gingivalis A 7436 lipopolysaccharide concentrations (0, 0.003, 0.03, 0.3 and 3.0 micrograms/ml) as compared to non-diabetic patients with gingivitis or adult periodontitis (p < 0.05). A significant difference in the dose response was also noted in the level of TNF alpha secreted as a function of P. gingivalis LPS concentrations between group A and B diabetics, as determined by two-way repeated measurements ANOVA (p < 0.05). Furthermore, there was no significant difference in the mean HbA1C between the two diabetic groups, and the TNF alpha level was not significantly associated with the HbA1C level within diabetic patients. These data suggest that the diabetic state results in an upregulated monocytic TNF alpha secretion phenotype (4.6-fold increase) which, in the presence of Gram-negative bacterial challenge, is associated with a more severe periodontal disease expression. In addition, approximately 40% (10 of 24) IDDM periodontitis patients in group B demonstrated a 62-fold elevation in TNF alpha secretion relative to non-diabetic gingivitis or periodontitis patients and a 13.5-fold increase relative to IDDM group A (gingivitis or mild periodontitis) patients.

Adult↗
PubMed1997

Inflammatory mediator response as a potential risk marker for periodontal diseases in insulin-dependent diabetes mellitus patients.

The gingival crevicular fluid (GCF) and monocytic secretion of prostaglandin E2 (PGE2) and interleukin 1 beta (IL-1 beta) were measured in a group of 39 insulin-dependent diabetes mellitus (IDDM) patients and 64 systemically healthy individuals. Diabetics were divided into Group A (gingivitis or mild periodontal disease) and Group B (moderate or severe periodontal disease). Diabetics had significantly higher GCF levels of both PGE2 and IL-1 beta as compared to non-diabetic controls who were matched with regard to periodontal disease severity (P < 0.00001 and P = 0.0005, respectively). Within the diabetic population, the GCF levels of these inflammatory mediators were almost 2-fold higher in Group B as compared to Group A (P = 0.01, P = 0.006, respectively for GCF-PGE2 and IL-1 beta). Furthermore, diabetics as a group had a significantly higher monocytic PGE2 and IL-1 beta production in response to various concentrations of both Escherichia coli and Prophyromonas gingivalis lipopolysaccharide (LPS) as compared to non-diabetic patients with adult periodontitis (P = 0.0001). LPS dose-response curves demonstrated that monocytes from Group B diabetics produced approximately 3 times more PGE2 than Group A monocytes; however, there was no significant difference in monocytic IL-1 beta secretion within the IDDM patients. The levels of GCF or monocytic mediators did not correlate with age, race, or glycosylated hemoglobin (HbA1C) levels. Our data suggest that the high GCF and monocytic secretion of PGE2 and IL-1 beta in IDDM patients may be a consequence of a systemic response trait and that the presence of Gram-negative infections such as periodontal diseases may interact synergistically to yield high local levels of these mediators and a more severe periodontal condition.

Adult↗
PubMed1997

Prevalence of selected chronic conditions: United States, 1990-1992.

This report presents an update of the prevalence of selected chronic conditions in the United States. Its purpose is to provide prevalence data by age, sex and age, race and age, family income, and geographic region for major chronic condition systems. It further assesses the percent of selected conditions that cause activity limitation, the percent for which a physician was consulted, and the percent that caused hospitalization. Conditions with the highest prevalence and those causing the most disability days are also analyzed. Trends in prevalence rates for the conditions with highest prevalence are examined as well. Information for this report is based on data collected during the National Health Interview Survey (NHIS) for the years 1990, 1991, and 1992. This is a continuing nationwide survey of households for which a probability sample of the civilian noninstitutionalized population of the United States is interviewed by the U.S. Bureau of the Census regarding the health and other characteristics of each member of the household. The sample for the years 1990-92 was composed of 142,638 households containing 368,075 persons. Each household was administered one of six of the chronic conditions system lists. Deformities or orthopedic impairments was the most frequent chronic condition reported with almost 35 million conditions. Other conditions high in prevalence were chronic sinusitis, arthritis, and high blood pressure with annual averages of 33.7, 31.8, and 27.6 million conditions, respectively. Mental retardation and multiple sclerosis caused the highest percents of activity limitation among persons afflicted, 87.5 percent and 69.4 percent, respectively. Deformities and other orthopedic impairments, arthritis, and heart disease caused the highest numbers of restricted activity days and bed disability days per year, whereas, malignant neoplasms of the lung, bronchus, and other respiratory sites, caused the highest number of restricted activity days per year, per condition reported, 96.1 days. In little more than a decade, the prevalence rate from asthma has increased almost 50 percent and the rate from chronic bronchitis has increased 46 percent.

Adult↗
PubMed1996

Evaluation of ketorolac concentrations in plasma and gingival crevicular fluid following topical treatment with oral rinses and dentifrices.

Two clinical studies were conducted to determine the relative amounts of ketorolac detectable locally in the gingival crevicular fluid (GCF) and systemically in plasma after oral, topical drug administration. The rinse study compared topical administration of three concentrations of ketorolac tromethamine (0.1%, 0.5%, and 0.01%) in oral rinse formulations administered topically and a perorally administered capsule (10 mg), and the dentifrice study compared two concentrations of ketorolac in dentifrice formulations (0.15% and 1.0%) with a 0.1% oral rinse, all treatments administered topically. The dose-corrected systemic availability of the three oral rinses evaluated in the rinse study relative to the peroral capsule was about 15%. However, the ratios of the observed maximum GCF ketorolac concentration to maximum plasma ketorolac concentration ranged from 22 to 49, compared to less than 1 for the peroral ketorolac capsule. Using this ratio as an estimate of the ability of a treatment to target the drug to the gingival tissue, these data indicate that the ketorolac oral rinses achieved greater delivery of drug to the gingival tissue (presumed site of action for periodontitis) with a lower systemic drug load than peroral administration of a ketorolac capsule. The dose-corrected relative systemic bioavailabilities for the dentifrice treatments with respect to the 0.1% rinse in the dentifrice study were 59.2% and 86.4% for the 1.0% and 0.15% dentifrices, respectively, indicating that significantly less ketorolac was systemically available from the two dentifrices relative to the oral rinse. The relative bioavailabilities of ketorolac in the GCF after dosing with the dentifrice formulations with respect to the rinse were 89.1% for the 1.0% dentifrice and 19.7% for the 0.15% dentifrice. Thus, the 1.0% dentifrice appears to provide statistically equivalent levels of ketorolac to the gingival tissue as the 0.1% oral rinse with significantly less systemic exposure. The T1/2 of ketorolac in the GCF was about 0.5 h for all three treatments, which is significantly less than the plasma half-life of about 5.3 h. These data suggest that GCF levels of ketorolac should remain above the IC50 for PGE2-stimulated IL-1 bone resorption for about 7 h following treatment, assuming continuation of the first-order elimination observed over the first two postdosing hours. We conclude that oral rinses and dentifrices are effective and preferred vehicles for administration of ketorolac for use in treatment of periodontitis.

Administration, Topical↗
PubMed1996

Reduction of postburn hyperalgesia after local injection of ketorolac in healthy volunteers.

BACKGROUND: Nonsteroidal antiinflammatory drugs may be particularly effective against prostaglandin-mediated, post-injury hyperalgesia and related inflammatory pain. However, their usefulness may be limited by their systemic side effects. The current study determined if local effectiveness can be achieved by low-dose intradermal nonsteroidal antiinflamatory drug administration. METHODS: Ten healthy volunteers were asked to make magnitude estimations of the pain induced by a contact thermal stimulator at 1 degree C increments between 43 and 51 degrees C at three 1 x 1 cm study sites on each forearm during three study phases:(1) baseline; (2) after pretreatment with 10 microl 0.9% saline (n=1 site on each forearm), 0.3 mg ketorolac (n=1 on each forearm), or nothing (n=1 on each forearm); and (3) after "injury" by a mild burn at the ketorolac- and saline-treated sites on one arm or by injection of 10 nmol bradykinin at all three sites on the other arm. The effects of pretreatment on the pain induced by thermal testing were assessed using repeated-measures analysis of variance. RESULTS: Pretreatment with ketorolac had a selective effect on the postburn injury hyperalgesia, reducing the increase in pain intensity (P<0.05) but not the decline in pain threshold. It had no effect on the responses to thermal stimuli before injury or on the pain of burning, which were similar at ketorolac- and saline-treated sites. The effect of pretreatment with ketorolac on bradykinin-induced hyperalgesia was not achieved after bradykinin injection at sites pretreated with saline as well as ketorolac.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1996

The effect of ketoprofen creams on periodontal disease in rhesus monkeys.

Ketoprofen creams were evaluated for the treatment of periodontal disease in a placebo-controlled, double-blind study in the rhesus monkeys, Macaca mulatta. Two formulations containing ketoprofen (1%), with or without vitamin E, were evaluated against appropriate controls (8 monkeys per group). Two weeks prior to treatment, the animals received prophylaxis on only the left side of the mouth (spontaneous model). Selected teeth on the right side of the mouth were ligated (ligature model). The creams were administered to the gingiva once daily at a standard dose of 1.8 ml per monkey for 6 months. Clinical assessments were made 2 wk before initiation, at baseline and 1, 2, 3 and 6 months post-treatment. The clinical parameters included plaque formation, gingival redness, edema, bleeding on probing and Ramfjord Attachment Level measurements (RAL). Radiographs were taken at 2 wk before initiation, baseline and at 3 and 6 months post-treatment. Digital, subtraction radiography was used to measure vertical linear bone loss along the interproximal root surfaces of the left and right mandibular first molars. Gingival crevicular fluid (GCF) was collected for biochemical assays on PGE2, TxB2, LTB4, IL-1 beta and TNF alpha. There were no significant differences among groups with respect to gingival indices. Radiographic data demonstrated significant positive effects on bone activity in both groups treated with ketoprofen formulations with improvement over time in the ligature model (0.01 < or = p < or = 0.04). The placebo group exhibited bone loss of 1.96 +/- 0.48 and 1.40 +/- 0.56 mm per site at 3 and 6 months, respectively. The group treated with ketoprofen cream showed an apparent bone gain of 0.28 +/- 0.41 and 0.78 +/- 0.47 mm per site at 3 and 6 months, respectively. The group treated with ketoprofen cream containing vitamin E showed a mean bone loss of 0.41-0.48 mm per site at 3 months with improvement to an apparent bone gain of 0.31 +/- 0.44 mm per site at 6 months. The biochemical data demonstrated early and significant suppression of GCF-LTB4 by both ketoprofen formulations at 1 month, which preceded the significant suppression of GCF-PGE2 at 2 and 3 months in the ligature model (p < 0.003) and at 2 to 6 months in the spontaneous model (p < 0.02). We conclude that ketoprofen at 1% level in suitable topical vehicles can effectively inhibit GCF-LTB4 and GCF-PGE2 and positively alter alveolar bone activity in the ligature-induced model of periodontitis in the monkey.

Administration, Topical↗
PubMed1996

The selective B-A conformational transition of the central dinucleotide (CpG) segment of d(CAATCCGGATTG)2 induced by delta-Co(en)3(3+).

The binding of Co(NH3)6(3+), delta-Co(en)3(3+) and delta-Rh(en)3(3+) to the dodecanucleotide d(CAATCCGGATTG)2 has been studied by 1H NMR. Addition of Co(NH3)6(3+), delta-Co(en)3(3+) or delta-Rh(en)3(3+) to d(CAATCCGGATTG)2 induce a similar pattern of chemical shift movements of the dodecanucleotide base protons. Analysis of the chemical shift changes as a function of added metal-ion complex shows that the binding affinity for d(CAATCCGGATTG)2 decreases in the order: delta-Co(en)3(3+) > delta-Rh(en)3(3+) > Co(NH3)6(3+). Addition of a saturating ratio of delta-Co(en)3(3+) to d(CAATCCGGATTG)2 induces a selective B to A type-DNA transition for the central CpG segment of the dodecanucleotide, with all other nucleotide residues maintaining the B-type conformation.

Base Sequence↗
PubMed1996

Health and selected socioeconomic characteristics of the family: United States, 1988-90.

National estimates of average annual health indexes for the civilian noninstitutionalized population of the United States are presented in this report according to selected socioeconomic characteristics of the family. These estimates are based on data from the National Health Interview Survey (NHIS) in 1988, 1989, and 1990. Health indexes presented include percent limited in activity; percent with fair or poor respondent-assessed health status, restricted activity days, bed disability days, work-loss days, and school-loss days; percent with a physician contact in past year; numbers of annual physician contacts per person per year; percent with a hospital episode in the past year; days per short-term hospital stay; and incidence of acute conditions. This report includes the findings that persons living by themselves reported a higher percent of limitations in activity, high rates of disability days, more physician contacts per year, and a higher incidence rate from acute conditions than all persons 45-64 years of age. Persons in all four age groups reported higher percents with limitations of activity and higher percents with fair or poor health status in families in which the educational level of the responsible family adult member was less the 12 years than in families where the responsible adult was better educated. Both males and females, and white persons and black persons, in each of the age groups 18 years and over who were living with a spouse reported lower percents of limitations in activity than did persons living in other family relationships.

Absenteeism↗
PubMed1995

Halothane effects on low-threshold receptive field size of rat spinal dorsal horn neurons appear to be independent of supraspinal modulatory systems.

Recent evidence strongly supports the importance of spinal sites of action for the ability of general anesthetic agents to block response to noxious stimuli. This study was designed to examine possible spinal anesthetic effects on non-noxiously evoked activity. Three groups of rats were prepared for acute experiments in which the response of spinal dorsal horn neurons to low threshold receptive field (RF) stimulation was evaluated. In each animal in each group extracellular activity was recorded from a single spinal dorsal horn neuron. A low-threshold RF of each neuron and, at times, the sensitivity to low-threshold stimulation of multiple sites in the RF were determined under baseline conditions (light anesthesia or decerebrate). In Group 1, reversible cooling of the thoracic spinal cord in the presence of either 0.5% or 1% halothane anesthesia caused no change in RF size. However, an increase from 0.5% to 1% halothane caused a 53% decrease in RF size both in the presence and absence of a reversible cold block of the spinal cord. In Group 2, animals with spinal cords transected at the thoracic level had a similar change in low-threshold receptive field size (52%) when halothane concentrations were increased from 0.5% to 1%. Testing sensitivity within the RF areas indicated that the silenced areas at the fringe of the receptive field could still elicit activation of spinal dorsal horn neurons but at a higher threshold. In the final group of animals, decerebration and spinal cord transection allowed us to compare effects of 0.5% and 1% halothane with an anesthetic free baseline. Here, again, a dose-dependent reduction in RF area was observed although the baseline RFs were significantly smaller than those in Groups 1 and 2. These results demonstrate that the reduction in low-threshold receptive field size due to the administration of the inhalation anesthetic halothane occurs in the absence of descending modulation from supraspinal sites. This implicates the spinal dorsal horn as a potentially important site of action for general anesthetics. These results also support the spinal cord as an important tool to study the pharmacology responsible for anesthetic effects on sensory processing.

Animals↗
PubMed1995

Role of WDR neurons in a hind limb noxious heat evoked flexion withdrawal reflex.

Behavioral experiments and neurophysiological experiments, the two major types of preclinical studies which have paved the way for the development of spinal analgesia were compared under identical conditions utilizing the same animals. The results demonstrate that the activation of the wide dynamic range (WDR) neurons preceded the behavioral withdrawal reflexes, and that the activation of the WDR neurons occurred at lower stimulus temperature than that for the withdrawal reflex. The results suggest that the neuronal activation began before the behavioral reflex but also that the firing frequency of the WDR neurons at the time of the withdrawal reflex could not distinguish between non-noxious and noxious stimuli. Further study is needed to elucidate the neuronal mechanisms of the activation of the behavioral reflex.

Animals↗
PubMed1995

Anesthetic actions within the spinal cord: contributions to the state of general anesthesia.

The behavioral state known as general anesthesia is the result of actions of general anesthetic agents at multiple sites within the neuraxis. The most common end point used to measure the presence of anesthesia is absence of movement following the presentation of a noxious stimulus. The actions of general anesthetics within the spinal cord have been shown to contribute significantly to the suppression of pain-evoked movements, an important component of clinical anesthesia. Studies in the spinal cord are likely to increase our understanding of the pharmacology by which general anesthetics alter the transmission of somatomotor information. It now appears that the pharmacology responsible for the production of anesthesia is agent- and site-selective, and not the result of a unitary mechanism of action.

Anesthesia, General↗
PubMed1995

Intrathecal prostaglandin E1 produces a long-lasting allodynic state.

The existence of prostaglandin (PG) receptors in the spinal cord has been demonstrated, but their role in sensory processing is not yet well defined. PGE1 is widely used clinically as a vasodilator. The present study was designed to investigate the effects of intrathecally administered PGE1 on the transmission of different types to sensory information, including that associated with noxious somatic, noxious visceral, and non-noxious somatic stimulation. The tail-flick (TF) test was employed to measure responses to noxious somatic stimuli, and the colorectal distension test was used to examine responses to noxious visceral stimuli. Withdrawal response to mechanical pressure produced by Semmes-Weinstein mono-filaments (SWMs) was measured as an assessment of sensitivity to non-noxious mechanical somatic stimulation. TF latencies and colorectal distension thresholds decreased for a short time (10-20 min) following the intrathecal (i.t.) administration of both 100 ng or 500 ng of PGE1. In sharp contrast to these short duration effects, there was a long-lasting increase in agitation scores (allodynia) produced by 3 different intensities of SWMs (0.217, 0.745 and 2.35 g) after administration of PGE1. The changes in agitation scores to SWMs were dependent on the dose of PGE1 and the intensity of stimulation. This increase of agitation score was seen when PGE1 was administered through the i.t. catheter or by direct i.t. puncture and the increase lasted for at least 2 days after drug administration. Intrathecal administration of saline, however, did not produce any changes in TF latencies, colorectal distension thresholds, or agitation scores produced by SWMs. No significant histological difference was seen between spinal cords exposed to 500 ng PGE1 and saline 48 h after drug administration. These results demonstrate that PGE1 may trigger a hypersensitive (allodynic and/or hyperalgesic) state in sensory processing pathways at the spinal level. They also indicate that long-lasting changes in processing of non-noxious, but not noxious, information produced by PGE1 continues after the disappearance of the direct action of PGE1.

Akathisia, Drug-Induced↗
PubMed1995

Contrasting actions of intrathecal U50,488H, morphine, or [D-Pen2, D-Pen5] enkephalin or intravenous U50,488H on the visceromotor response to colorectal distension in the rat.

BACKGROUND: Visceral sensations are an important component of many clinical pain states. It is apparent that intrathecal pain relief may be more effective if appropriate combinations of drugs rather than a single agent can be used. The purpose of this study was to examine the relative contribution of opioid receptor subtypes to visceral antinociception using colorectal distension as a visceral pain model. METHODS: The minimum colorectal distending pressure necessary to evoke a visceromotor response (contraction of abdominal musculature) was determined before and after the administration of opioid agonists for the mu (morphine), delta ([D-Pen2, D-Pen5] enkephalin [DPDPE]), and kappa (U50,488H) opioid receptors. In addition to the three drugs administered intrathecally, U50, 488H was also administered intravenously. RESULTS: Morphine and DPDPE produced a reversible increase in threshold for activation of the visceromotor response (50% maximum possible effect [MPE] at intrathecal doses of 2.2 and 16.4 micrograms, respectively). The maximum intrathecal dose of U50,488H (100 micrograms) produced only a 20% MPE. Intravenous U50,488H produced a 50% MPE at a dose of 2.6 mg/kg. CONCLUSIONS: The results suggest that spinal mu- and delta- but not kappa-opioid receptors have a significant role in the modulation of visceral nociception induced by colorectal distension. In addition, the results indicate that activation of nonspinal kappa receptors may mediate visceral antinociception.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1995

Visceral antinociceptive effects of spinal clonidine combined with morphine, [D-Pen2, D-Pen5] enkephalin, or U50,488H.

BACKGROUND: Visceral pain is an important component of many clinical pain states. The perispinal administration of drug combinations rather than a single agent may reduce side effects while maximizing analgesic effectiveness. The purpose of this study was to examine the nature of interactions between an alpha 2-adrenergic agonist (clonidine) and a mu-opioid agonist (morphine), a delta-opioid agonist ([D-Pen2, D-Pen5] enkephalin [DPDPE]), or a kappa-opioid agonist (U50,488H). METHODS: Colorectal distension was used to elicit a nociceptive visceromotor response (contraction of abdominal musculature) in rats. The ability of intrathecally administered clonidine alone or in combination with morphine, DPDPE, or U50,488H to alter thresholds for the production of the visceromotor response was examined. RESULTS: Clonidine produced dose-dependent reduction in threshold. U50,488H, at the doses tested, showed no synergistic interaction with clonidine. CONCLUSIONS: Spinal combinations of alpha 2-adrenergic and mu- or delta- but not kappa-opioid agonists may be beneficial in the control of visceral pain.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗