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P Simons

Publications and source records attributed to P Simons.

27 records · Page 2Linked to original sources
PubMed1987

Validity of a hinged constant force probe and a similar, immobilised probe in untreated periodontal disease.

The validity of a hinged constant force probe (0.25 N) was compared with that of a similar but immobilised instrument, using the same interchangeable tip for both (0.64 mm diameter; 2 mm divisions). 60 sites were measured on teeth which were extracted subsequently, in patients with untreated periodontal disease, and the connective tissue attachment level was used as validity criterion. The clinical measurements of both probes correlated well with each other, but they differed significantly from the post-extraction connective tissue attachment level measurements, indicating a point 1.2 mm coronally to this, on average. A companion investigation of intra-operator probing depth reproducibility with the 2 probes, was undertaken in 14 patients, at 2 visits separated by 1 week in each case. All patients had untreated periodontal disease. A difference between probes was found at the first visit, but not at the second; the immobilised probe showed a difference between visits, reducing mean probing depth slightly at the second; when the immobilised probe was used first, there was a difference between probes. Further analysis of the results indicated that there was greatest agreement between probes when the constant force probe had been used before the immobilised probe at the second visit. The results suggested that these probes indicated a point above the connective tissue attachment level, related to pocket morphology, and that there was a moderate learning effect due to operator use of the constant force probe, which modified use of the immobilised probe.

Connective Tissue↗
PubMed1986

Response of the local heme environment of (carbonmonoxy)hemoglobin to protein dehydration.

The effects of protein dehydration upon the equilibrium and dynamic properties of the heme active site in human hemoglobin (HbA) have been probed by resonance Raman scattering. Spectra of equilibrium carbonmonoxy-HbA and the photolytic heme transient species generated within 10 ns of ligand photolysis have been obtained from thin films of protein in various stages of dehydration. These data provide detailed information concerning the response of the heme and its bonding interactions with both the proximal histidine and carbon monoxide as a function of protein hydration. For protein hydration levels of 0.4-1.0 g of H2O/g of protein, our results indicate that the C = O stretching mode of carbonmonoxy-HbA is dramatically affected by protein hydration levels, thus corroborating the infrared results of Brown et al. [Brown, W. E., Sutcliffe, J. W., & Pulsinelli, P. D. (1983) Biochemistry 22, 2914-2923]. However, we find that both heme skeletal modes and the Fe-C bond strength are largely insensitive to dehydration. Moreover, the proximal pocket geometry (as reflected in the behavior of the Fe-proximal histidine stretching mode) immediately following ligand photolysis was found to be very similar to that of R-state solution hemoglobin. At protein hydration levels below the theoretical monolayer limit, small changes in the resonance Raman spectra of both equilibrium HbCO and the transient heme species generated subsequent to ligand photolysis are detected. These include broadening of the Fe-C stretching mode in equilibrium HbCO and a small shift to lower frequency of the Fe-His mode in the photolytic transient species.(ABSTRACT TRUNCATED AT 250 WORDS)

Carboxyhemoglobin↗
PubMed1983

CGP-12177. A hydrophilic beta-adrenergic receptor radioligand reveals high affinity binding of agonists to intact cells.

A new, hydrophilic beta-adrenergic receptor radioligand, (+/-)-[3H]CGP-12177 (4-(3-tertiarybutylamino-2-hydroxypropoxy)-benzimidazole-2-on hydrochloride), was synthesized and radiolabeled to 40 Ci/mmol. The nonspecific binding of this compound to turkey erythrocyte ghosts and C6 glioma cell membranes was less than 5% of the total binding at five times the appropriate KD. Binding assays of intact C6 glioma cells also showed low nonspecific binding, less than 20% of the total binding at five times the appropriate KD. The affinities of the antagonists (-)- and (+)-propranolol as well as of the agonist (-)-isoproterenol were examined by their potency to displace various radioligands from intact C6 glioma cell and membrane preparations. With membrane preparations, both [3H] CGP-12177 and [3H]dihydroalprenolol (DHA) were displaced stereospecifically by the antagonists (-)- and (+)-propranolol and the agonist (-)-isoproterenol. With whole cells, [3H]CGP-12177 and [3H]DHA behaved differently. [3H]DHA and [3H]carazolol could be stereospecifically displaced by antagonists but only partially displaced by agonists, while [3H]CGP-12177 could be completely displaced by both antagonists and agonists as in membranes. In contrast to [3H]CGP-12177, the lipophilic ligand [3H]DHA is actually taken up by cells. The inability of agonists to displace lipophilic radioligands from receptors on intact cells may not be due to a low affinity of agonists for receptors on cells, but to an agonist-induced change in the receptors which renders them inaccessible to hydrophilic agonists and antagonists. This change is likely to be their internalization into the cell.

Adrenergic beta-Antagonists↗
PubMed1982

Rapid and reversible disappearance of beta-adrenergic cell surface receptors.

The water soluble beta-adrenergic ligand [3H]CGP-12177 was used to measure the cell surface receptors in intact cells. In two cell lines, C6 glioma and WEHI 7 lymphoma cells, -50% of the cell surface receptors disappear within minutes of incubation of the cells with isoproterenol. The receptors can still be detected in homogenates and reappear on the cell surface when cells are washed and reincubated at 37 degrees C. The data agree with a disappearance of the receptors from the cell surface by an agonist-mediated endocytosis.

Animals↗
PubMed1975

The disposition and metabolism of I.C.I. 58,834 (viloxazine) in animals.

1. 2-(2-Ethoxyphenoxymethyl-2,3,5,6-tetrahydro-1,4-oxazine (I.C.I. 58,834) has been prepared in three different 14C-labelled forms and its absorption, distribution, metabolism and elimination studied in six animals species. 2. In all species I.C.I. 58,834 was well absorbed after oral administration and extensively metabolized. Excretion via the kidney was the main route of elimination. 3. In the rat the major metabolic pathway is o-dealkylation and sulphate conjugation; the dealkylated metabolite was detected in brain extracts. A novel type of polar metabolite was isolated from rat urine, apparently a conjugate with sulphate and hippurate. 4. The metabolic pathways in beagle dogs include hydroxylation of the phenyl ring (and subsequent conjugation), N-methylation, formation of the N-methyl-N-oxide, and oxidation of the oxazine ring. 5. Maximum blood levels of I.C.I. 58,834 in dogs were unchanged during eight weeks daily administration and the half-life was 2.5-3 h. I.C.I. 58,834 is the main component in dog blood. Rat serum contains mainly conjugates of dealkylated I.C.I. 58,834 and the parent compound is a minor component. 6. None of the metabolites has significant CNS activity and activity observed following administration of I.C.I. 58,834 is due primarily to the parent compound.

Animals↗
PubMedDate not supplied

Cost effectiveness of an allergy consultation in the management of asthma.

In a large Denver HMO, a retrospective study of asthma management was reviewed. Seventy moderate to severe asthmatic patients' charts were reviewed through April 1994. All patients admitted to the study had to be followed for at least 1 year by a primary care physician before the allergy evaluation (AE) and for at least one year of followup (F/U) after the AE. All patients had at least two acute care (ER) visits and/or one hospitalization before the AE. All primary care, AE, and F/U were done by staff physicians in the Kaiser Permanente system. The findings included 1) Forty-five percent decrease (308 to 169) in the number of sick care office visits (P = 0.0001); 2) fifty-five percent decrease (266 to 118) in acute care visits (P = 0.0001); 3) sixty-seven percent decrease (34 to 11) in the number of hospitalizations after the AE (P = 0.001); 4) average hospital days before AE were four days and after AE, 2.5 days; 5) estimated cost saving of $145,500, or $2,100 per patient.

Acute Disease↗