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BACKGROUND: preoperative anxiety at induction and postoperative emergence delirium (ED) in children are associated with postoperative behavioral changes and adjustment disorders. This study's aim is to assess the value of the Child Behavior Checklist (CBCL) score in order to predict anxiety during induction and emergence delirium after anesthesia in children undergoing elective day-care surgery. METHODS: Anxiety at induction, assessed by the modified Yale Preoperative Anxiety Scale (mYPAS), was studied as outcome in 401 children (60.1% male, age range: 1.5-16 years). For 343 of these children (59.8% male, age range: 1.5-16 years) ED could be investigated postoperatively, as assessed by the Pediatric Anesthesia Emergence Delirium scale (PAED). Demographic data, healthcare contacts, anesthesia and surgical data were registered. Preoperative emotional/behavioral problems, during the 6 months prior to surgery, were assessed by the CBCL. Hierarchical, multiple regression was used to test whether anxiety and ED could be predicted by CBCL scores. RESULTS: Children with a higher CBCL score on preoperative internalizing problems (e.g. anxious/depression) showed preoperative more anxiety at induction (P=0.003). A higher CBCL score on preoperative emotional/behavioral problems was not associated with ED. CONCLUSION: The CBCL predicted anxiety at induction but not ED.

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Self-concept is a widely examined construct in the area of psychiatric disorders. This study compared the Physical Self-Description Questionnaire (PSDQ) scores of adolescents with psychiatric disorders (N=103) with the results of a matched group of non-clinical adolescents (N=103). Self-concept and Physical self-concept were lower in the clinical than in the non-clinical group. Girls (N=59) scored lower than boys (N=44) in both groups. In the different diagnostic groups specific domains were affected in line with symptomatology, which has implications for therapy.

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BACKGROUND: The regeneration of gingival papillae after single-implant treatment is an area of current investigation. This study was designed to determine: 1) whether the distance from the base of the contact point to the crest of the bone would correlate with the presence or absence of interproximal papillae adjacent to single-tooth implants, and 2) whether the surgical technique at uncovering influences the outcome. METHODS: A clinical and radiographic retrospective evaluation of the papilla level around single dental implants and their adjacent teeth was performed in the anterior maxilla in 26 patients restored with 27 implants. Six months after insertion, 17 implants were uncovered with a standard technique, while 10 implants were uncovered with a technique designed to generate papilla-like formation around dental implants. Fifty-two papillae were available for clinical and radiographic evaluation. The presence or absence of papillae was determined, and the effects of the following variables were analyzed: the influence of the 2 surgical techniques; the vertical relation between the papilla height and the crest of bone between the implant and adjacent teeth; the vertical relation between the papilla level and the contact point between the crowns of the teeth and the implant; and the distance from the contact point to the crest of bone. RESULTS: When the measurement from the contact point to the crest of bone was 5 mm or less, the papilla was present almost 100% of the time. When the distance was > or = 6 mm, the papilla was present 50% of the time or less. The mean distance between the crest of bone and the most coronal papilla level (interproximal soft tissue height) was 3.85 mm (SD = 1.04). When comparing the conventional and modified surgical technique, the relation shifted from 3.77 mm (SD = 1.01) to 4.01 mm (SD = 1.10), respectively. CONCLUSIONS: These results clearly show the influence of the bone crest on the presence or absence of papillae between implants and adjacent teeth. The data also show a positive influence for the modified surgical technique, aimed at reconstructing papillae at the implant uncovering.

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With the latest developments of the Procera system, all-ceramic crowns have become an attractive solution to provide functional and esthetic rehabilitation on teeth and dental implants. The Procera AllCeram crown and Procera Abutment embrace the concept of computer-assisted design and computer-assisted machining (CAD/CAM) and can be used together for optimal esthetic result. The purpose of this case report was to illustrate the advantages of these new components for complex anterior rehabilitation. Three natural teeth and a Procera Abutment were restored using four Procera AllCeram crowns. Treatment planning and esthetic benefits are discussed.

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A new soft tissue flap design technique, called "the palatal sliding strip flap" (PSSF), has been developed to improve the soft tissue surgical results at stage 2 implant surgery. The purpose of this flap design is to help form papillae between implants and between natural teeth in the anterior area of the maxilla. The flap is designed and managed so that the palatal attached mucosa slides in a labial direction to create papillae and at the same time augment the labial ridge. This surgical approach is valid, predictable, and has a low risk-to-benefit ratio. This new flap design is indicated for a variety of clinical situations, especially for the problematic maxillary soft tissue reconstruction around teeth and implants.

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The synthetic peptide SNX-111 corresponding to the sequence of the omega-conopeptide MVIIA from the venom of the marine snail Conus magus is a highly potent and selective antagonist of N-type calcium channels. We have synthesized and characterized a large number of analogs of SNX-111 in order to elucidate the structural features of the peptide involved in blocking N-type calcium channels. Comparison of the binding of SNX-111 and its analogs to rat brain synaptosomal membranes rich in N-type channels revealed that, among the four lysines and two arginines in the molecule, lysine in position 2 and arginines at position 10 and 21 are important for the interaction of SNX-111 with N-type channels. The importance of the middle segment from residues 9 through 14 for this binding interaction was revealed by substitution of the individual residues as well as by the construction of hybrid peptides in which the residues 9-12 in SNX-111 and another conopeptide, SNX-183, corresponding to a peptide SVIB from Conus striatus, were interchanged. Introduction of the sequence SRLM from SNX-111 in place of RKTS in position 9-12 in SNX-183 resulted in a 38-fold increase in affinity.

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Motivating burned children to participate actively in rehabilitation at the burn unit demands many creative ideas. To avoid resistance from the child towards the exercises, it is important to offer a variety of techniques. A new play technique is outlined here, based on the use of video games, that is capable of motivating and stimulating children of all ages--even the youngest--towards active participation in rehabilitation.

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[3H]Dihydroergotamine (DE) labels a population of binding sites in rat brain membranes with an affinity of approximately 70 pM in both hippocampus (maximal binding at saturation [Bmax] = 340 fmol/mg of protein) and cerebral cortex (Bmax = 250 fmol/mg of protein). Specific binding typically comprises about 97% of total binding at the Kd of the radioligand when nonspecific binding is determined in the presence of 100 nM unlabeled DE. Association kinetics at 37 degrees C are consistent with a uniform association rate constant for all sites labeled. Specific binding is completely reversible with addition of excess unlabeled DE, but dissociation does not proceed with simple first-order kinetics, suggesting the presence of more than one discrete binding site. Competition studies with selective drugs reveal alpha adrenergic, 5-HT1A and 5-HT1B components of [3H]DE specific binding. When phentolamine (500 nM) is included to block alpha receptors and DPAT (100 nM) or spiroxatrine (500 nM) is included to block 5-HT1A receptors, specific binding is exclusively to sites with drug affinities characteristic of 5-HT1B receptors. Under these 5-HT1B-selective conditions, [3H]DE binding is about 90% specific, with a Kd of about 50 to 60 pM and a Bmax of 96 fmol/mg of protein in hippocampus and 77 fmol/mg of protein in cortex. [3H]DE binding to 5-HT1B sites is very slowly dissociable, with a T1/2 of greater than 2 h at 37 degrees C. 5-HT1B antagonists and DE itself yield competition curves at [3H]DE-labeled 5-HT1B sites that are adequately fit assuming a single site in nonlinear regression analysis. Competition by the agonists 5-HT and RU 24969 at 5-HT1B sites are often best described by two site fits. Addition of 100 microM guanylyl 5'-imidodiphosphate appears to convert nearly all 5-HT1B sites to those having low affinity for agonists while having a much smaller effect on the binding of [3H]DE. This suggests that the 5-HT1B site exists in two interconvertable agonist affinity states and is yet another member of the G-protein-linked receptor family. In agreement with previous studies using other radioligands, no 5-HT1B sites can be detected in bovine, porcine or human hippocampus membranes.

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[3H]-5-Hydroxytryptamine ([3H]-5-HT) decomposes rapidly when exposed to air in solution at physiological pH if antioxidants are not present. The decomposition products appear to bind to two saturable sites on brain membranes (apparent Kd values = 1-2 and 100-1000 nM). This binding mimics "specific" ligand/receptor binding in that it is inhibited by 10 microM unlabeled 5-HT. This inhibition is not competitive, but rather is due to the prevention of [3H]-5-HT breakdown by excess unlabeled 5-HT. Unlike genuine ligand/receptor binding, the binding of [3H]-5-HT breakdown products is essentially irreversible and does not display a tissue distribution consistent with binding to authentic 5-HT receptors. [3H]-5-HT decomposition can be eliminated by the inclusion of 0.05 to 5 mM ascorbic acid. At these concentrations ascorbic acid is not deleterious to reversible [3H]-5-HT binding. When [3H] 5-HT exposure to air occurs in the presence of brain membranes, the apparent antioxidant activity of brain membranes themselves affords protection against [3H]-5-HT degradation equal to ascorbic acid. This protection is effective below final [3H]-5-HT concentrations of 10 nM. Above 10 nM [3H]-5-HT, addition of ascorbic acid or other antioxidants is necessary to avoid the occurrence of additional low affinity (apparent Kd = 15-2000 nM) binding sites that are specific but nonetheless irreversible. When care is taken to limit [3H]-5-HT oxidation, the only reversible and saturable specific binding sites observed are of the 5-HT1 high affinity (Kd = 1-2 nM) type. Radioligand oxidation artifacts may be involved in previous reports of low affinity (Kd = 15-250 nM) [3H]-5-HT binding sites in brain membrane preparations.

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At the University Burn Unit in Leuven (Belgium), we have been working for 4 years now with a multidisciplinary reintegration program. Our team consists of a plastic surgeon (head of the unit), a physical therapist, a social worker and a child psychiatrist. We set up family, context-oriented counselling for the families of seriously burned patients. In this paper, we would like to illustrate some aspects of the importance of facial scars in our society as well as the consequences of such scars for the families of patients. These are 2 essential aspects which have to be taken into account so that the counsellors and family do not reach a deadlock. We discuss how this therapy can be applied. Cooperation with the school is a keystone in the application of such therapy. The teacher is involved as a reflection of the feelings of the parents. Via this intermediary they learn how to cope with their feelings and to talk about them. The team has experienced this as an important step in the construction of family therapy.

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Previous results in various in vitro systems suggest that prostaglandin endoperoxide synthetase (PES) could serve as either an alternative or an additional enzyme to the cytochrome P-450-dependent monooxygenases for the formation of mutagenic, cell-transforming, and DNA-binding metabolites of carcinogens. To test this hypothesis in vivo, we examined the effect of PES inhibitors on benzo(a)pyrene (BP)-induced pulmonary adenoma and BP metabolite:DNA adduct formation in A/HeJ mice. Animals were treated with a dosage regimen of aspirin which inhibited PES but had no effect on the cytochrome P-450-dependent oxidation of 7,8-dihydrodihydroxybenzo(a)pyrene. Aspirin did not significantly alter the number of pulmonary adenomas per mouse at either dose of BP (6.0 and 3.0 mg per mouse, administered twice, 2 weeks apart). In addition, aspirin treatment did not depress the in vivo formation of BP metabolite:DNA adducts in lung or liver at either dose of BP (6.0 and 0.06 mg/mouse). The lower dose of BP was used in the adduct study to assess the effect of aspirin at a more environmental exposure level of BP. Treatment with indomethacin, another PES inhibitor, also did not reduce the pulmonary BP metabolite:DNA adduct levels. The failure of PES inhibitors to reduce the number of pulmonary adenomas and BP metabolite:DNA adduct levels suggests that cooxidation of BP during prostaglandin biosynthesis may not play a significant role in BP-induced pulmonary adenomas.

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In this study, the formation of benzo(a)pyrene (BP) metabolite:DNA adducts in lung, liver, and forestomach of control and butylated hydroxyanisole (BHA)-treated (5 mg/g diet) female A/HeJ mice was examined as a function of BP dose (p.o.), ranging from 2 to 1351 mumol/kg. The major identified adduct in each tissue at each dose was the (+)-7 beta,8 alpha-dihydroxy-9 alpha,10 alpha-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene (BPDEI):deoxyguanosine adduct. A 7 beta,8 alpha-dihydroxy-9 beta,10 beta-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene:deoxyguanosine adduct, a(-)-BPDEI:deoxyguanosine adduct, and an unidentified adduct were also observed. In lung and liver of untreated animals, the dose-response curves for BPDEI:DNA adduct levels were sigmoidal. In forestomach, there was no indication of saturation of DNA binding over the BP dose range examined. The dose-response curves became linear as BP dose approached zero and thus, no threshold dose existed below which binding of BPDEI to DNA did not occur, at least in lung, liver, and forestomach of these mice. In forestomach, the dose-response curve for BPDEI:DNA adducts in BHA-treated mice, 0.5% of diet for 2 weeks, was parallel to the curve for control animals and thus, the inhibition (45%) of adduct formation is independent of BP dose. In contrast, BHA treatment diminished the curvilinear nature of the dose-response curves for BPDE adducts in lung and liver. The inhibition of BPDEI:DNA adduct formation by BHA in lung and liver was dose dependent. The inhibition of lung (68%) and liver (82%) adduct formation was highest at a BP dose of 270 mumol/kg. As the BP dose approached zero, the inhibition of BPDEI:DNA adduct formation by BHA decreased with BP dose and approached values of approximately 40% (lung) and 55% (liver). The dose dependency of the binding of BP metabolites to protein was also examined. BPDEI:DNA adduct concentrations ranged from 2 to 10% of protein binding concentrations in liver of untreated animals, from 3 to 7% in forestomach, and from 5 to 7% in lung. The dose-response curves for protein binding of BP metabolites in lung and liver from BHA-treated animals were essentially parallel to those in control animals and thus, the inhibition of protein binding by BHA treatment had no dose dependency in these organs. No consistent BHA effect was observed on the amount of binding of BP metabolites to forestomach protein.

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A method has been developed for the emergency estimation of paracetamol using high performance liquid chromatography. The sample required is 100 microliters of plasma; the use of a micro-centrifuge reduces the total time for the estimation to 5 min from the receipt of the blood specimen. The method has been compared with a standard UV method.

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The plasma concentrations and urinary excretion of paracetamol and its glucuronide, sulphate, cysteine and mercapturic acid conjugates were measured in eight normal subjects, eight patients with mild liver disease and seven patients with severe liver disease following an oral dose of 1.5 g of paracetamol. The mean plasma paracetamol half-life was similar in normal subjects (2.43 h +/- 0.19) but was significantly prolonged in all patients with severe liver disease (4.25 h +/- 1.15:p = less than 0.001). Prolongation of the paracetamol half-life was related to reduced plasma albumin and increased prothrombin time. The mean ratios of plasma concentrations of unchanged paracetamol to paracetamol glucoronide and sulphate were significantly greater in patients with sever liver disease than the normal subjects. There were no significant differences in the overall 24-h urinary excretion of paracetamol and its glucuronide, sulphate, cysteine and mercapturic acid conjugates in the three groups. The glutathione conjugation of paracetamol did not seem to be impaired in patients with severe liver disease as evidence by the production of normal amounts of the cysteine and mercapturic acid conjugates. There is thus no evidence that they are at increased risk of hepatotoxicity when given a single therapeutic dose of paracetamol.

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Methods for the estimation of plasma paracetamol which depend on acid hydrolysis to p-aminophenol without a prior extraction step also measure inactive metabolites which are present in high concentrations. The extent of the overestimate obtained with such methods was determined using 24 samples from patents after paracetamol overdosage. There was a positive error of between 40 and 700% compared with a high-performance liquid chromatography reference method which measured only unchanged paracetamol. These non-specific methods should not be used to determine the need for specific therapy in patients with paracetamol poisoning.

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Fifteen patients with paracetamol (acetaminophen) poisoning were treated with intravenous N-acetylcystein (300 mg/kg given over 20 h). Mean admission and 4 h plasma-paracetamol concentrations were 262 and 369 microgram/ml, respectively. Liver-function tests remained normal or were only slightly disturbed in 11 of 12 patients treated within 10 h of paracetamol ingestion. Severe liver damage developed in the other patient and in the three in whom treatment was started more than 10 h after paracetamol ingestion. In contrast to cysteamine, N-acetylcysteine was very well tolerated and has the advantage of being available as a pharmaceutical preparation in a 20% sterile solution.

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