[Low-cost reconstructive treatment after resection of distal radius giant cell tumor]. / Tratamiento reconstructivo de bajo costo tras resección de tumor de células gigantes de radio distal.

INTRODUCTION: giant cell tumor (GCT) is a benign intramedullary bone tumor that frequently arises at the ends of long bones. After the distal femur and proximal tibia, the distal radius is the third most affected site with particularly aggressive tumors. Our objective is the presentation of the clinical case of a patient diagnosed with distal radius GCT classified in grade III of Campanacci who received a treatment adjusted to her economic possibilities. CASE REPORT: a 47-year-old female, without economic solvency and with some medical service. Treatment included block resection, reconstruction with distal fibula autograft, and radiocarpal fusion with blocked compression plate. Eighteen months later, the patient had good grip strength (80% on the healthy side) and had fine motor function in the hand. The wrist presented stability with pronation of 85o, supination of 80o, flexion-extension of 0o and a score of 6.7 in the DASH functional outcomes assessment questionnaire. His radiological evaluation five years after his surgery continued with no evidence of local recurrence and pulmonary involvement. CONCLUSION: the result in this patient, together with the published data, indicate that the block tumor resection technique, plus distal fibula autograft and arthrodesis with blocked compression plate provide an optimal result of functionality for the grade III distal radial tumor at low cost.

INTRODUCCIÓN: el tumor de células gigantes (TCG) es un tumor óseo intramedular benigno que surge con frecuencia en los extremos de los huesos largos. Después del fémur distal y la tibia proximal, el radio distal es el tercer sitio más afectado con tumores, particularmente agresivos. Nuestro objetivo es la presentación del caso clínico de una paciente con diagnóstico de TCG de radio distal clasificada en grado III de Campanacci que recibió un tratamiento ajustado a sus posibilidades económicas. REPORTE DE CASO: paciente femenino de 47 años, sin solvencia económica y sin ningún servicio médico. El tratamiento incluyó resección en bloque, reconstrucción con autoinjerto de peroné distal y artrodesis radiocarpiana con placa de compresión bloqueada. Dieciocho meses después, la paciente presentaba una buena fuerza de prensión (80% respecto al lado sano) y tenía una función motora fina en la mano. La muñeca presentó estabilidad con pronación de 85o, supinación de 80o, flexión-extensión de 0o y una puntuación de 6.7 en el cuestionario de evaluación de resultados funcionales DASH. Su evolución radiológica a cinco años después de su cirugía continuó sin datos de recidiva local y afectación pulmonar. CONCLUSIÓN: el resultado en esta paciente, junto con los datos publicados, indican que la técnica de resección tumoral en bloque, más el autoinjerto de peroné distal y la artrodesis con placa de compresión bloqueada proporcionan un resultado óptimo de funcionalidad para el tumor radial distal grado III a bajo costo.

Identification and quantification of aflatoxins and aflatoxicol from poultry feed and their recovery in poultry litter.

Aflatoxins (AF) are toxic fungal secondary metabolites and are known mycotoxins pathological to animals and humans. Poultry litter is frequently used as a food supplement for ruminants, and when poultry feed contains AF, the litter becomes contaminated as well, thus having an effect on livestock health. This study identified and quantified AF (AFB(1), AFB(2), AFG(1), and AFG(2)) from poultry feed and their recovery, together with their metabolites (AFM(1), AFM(2), AFP(1), and aflatoxicol) in litter. An experiment with 25 Hy-Line W-36 hens, in their second production stage, 121 wk old, was carried out. Hens were distributed in 3 groups placed in individual cages and 1 ration of 250 g of feed was given to each hen daily. Nine hens of the control group were fed with clean feed, without AFB(1); the other 2 experimental groups, with 8 hens each, were fed with 2 AFB(1) concentrations: 30 and 500 microg.kg(-1). The feed was replaced and weighed daily throughout a 7-d period to register the amount of feed consumed by the hens. Litter from each hen was collected, weighed, and dried individually. The chemical analysis of 40 g of each one of the 200 feed and 200 litter samples was chemically extracted and concentrated with immunoaffinity columns for total AF. To quantify AF, calibration curves for each AF were done by HPLC. Feed samples of the 3 groups presented significant difference with AFB(2) and AFG(2), whereas in litter samples, there were significant differences for AFG(2) in the 500 microg.kg(-1) group. Poultry litter had traces of AFM(1), AFM(2), AFP(1), and AFL with no significant differences among treatments. Aflatoxin B(1) prevalence in litter samples can cause damages in livestock because this mycotoxin reduces the digestibility of ruminant feed up to 67%.

c-Jun N-terminal kinase (JNK)-dependent internalization and Rab5-dependent endocytic sorting mediate long-distance retrograde neuronal death induced by axonal BDNF-p75 signaling.

During the development of the sympathetic nervous system, signals from tropomyosin-related kinase receptors (Trks) and p75 neurotrophin receptors (p75) compete to regulate survival and connectivity. During this process, nerve growth factor (NGF)- TrkA signaling in axons communicates NGF-mediated trophic responses in signaling endosomes. Whether axonal p75 signaling contributes to neuronal death and how signaling endosomes contribute to p75 signaling has not been established. Using compartmentalized sympathetic neuronal cultures (CSCGs) as a model, we observed that the addition of BDNF to axons increased the transport of p75 and induced death of sympathetic neurons in a dynein-dependent manner. In cell bodies, internalization of p75 required the activity of JNK, a downstream kinase mediating p75 death signaling in neurons. Additionally, the activity of Rab5, the key GTPase regulating early endosomes, was required for p75 death signaling. In axons, JNK and Rab5 were required for retrograde transport and death signaling mediated by axonal BDNF-p75 in CSCGs. JNK was also required for the proper axonal transport of p75-positive endosomes. Thus, our findings provide evidence that the activation of JNK by p75 in cell bodies and axons is required for internalization to a Rab5-positive signaling endosome and the further propagation of p75-dependent neuronal death signals.

ATP steal between cation pumps: a mechanism linking Na+ influx to the onset of necrotic Ca2+ overload.

We set out to identify molecular mechanisms underlying the onset of necrotic Ca(2+) overload, triggered in two epithelial cell lines by oxidative stress or metabolic depletion. As reported earlier, the overload was inhibited by extracellular Ca(2+) chelation and the cation channel blocker gadolinium. However, the surface permeability to Ca(2+) was reduced by 60%, thus discarding a role for Ca(2+) channel/carrier activation. Instead, we registered a collapse of the plasma membrane Ca(2+) ATPase (PMCA). Remarkably, inhibition of the Na(+)/K(+) ATPase rescued the PMCA and reverted the Ca(2+) rise. Thermodynamic considerations suggest that the Ca(2+) overload develops when the Na(+)/K(+) ATPase, by virtue of the Na(+) overload, clamps the ATP phosphorylation potential below the minimum required by the PMCA. In addition to providing the mechanism for the onset of Ca(2+) overload, the crosstalk between cation pumps offers a novel explanation for the role of Na(+) in cell death.

The RNA binding and transport proteins staufen and fragile X mental retardation protein are expressed by rat primary afferent neurons and localize to peripheral and central axons.

Neuronal proteins have been traditionally viewed as being derived solely from the soma; however, accumulating evidence indicates that dendritic and axonal sites are capable of a more autonomous role in terms of new protein synthesis. Such extra-somal translation allows for more rapid, on-demand regulation of neuronal structure and function than would otherwise be possible. While mechanisms of dendritic RNA transport have been elucidated, it remains unclear how RNA is trafficked into the axon for this purpose. Primary afferent neurons of the dorsal root (DRG) and trigeminal (TG) ganglia have among the longest axons in the neuraxis and such axonal protein synthesis would be advantageous, given the greater time involved for protein trafficking to occur via axonal transport. Therefore, we hypothesized that these primary sensory neurons might express proteins involved in RNA transport. Rat DRG and TG neurons expressed staufen (stau) 1 and 2 (detected at the mRNA level) and stau2 and fragile x mental retardation protein (FMRP; detected at the protein level). Stau2 mRNA was also detected in human TG neurons. Stau2 and FMRP protein were localized to the sciatic nerve and dorsal roots by immunohistochemistry and to dorsal roots by Western blot. Stau2 and FMRP immunoreactivities colocalized with transient receptor potential channel type 1 immunoreactivity in sensory axons of the sciatic nerve and dorsal root, suggesting that these proteins are being transported into the peripheral and central terminals of nociceptive sensory axons. Based on these findings, we propose that stau2 and FMRP proteins are attractive candidates to subserve RNA transport in sensory neurons, linking somal transcriptional events to axonal translation.

The effects of chemical or surgical deafferentation on [3H]-acetylcholine release from rat spinal cord.

Cholinergic modulation of nociceptive transmission through both nicotinic and muscarinic receptors in the spinal cord represents an important mechanism in pain signaling. However, what neuronal elements release acetylcholine and how release might change in response to deafferentation are unclear. The present studies demonstrated Ca++- and K+-dependent release of [3H]-acetylcholine from slices of regional areas of rat spinal cord. That [3H]-acetylcholine was synthesized from [3H]-choline was demonstrated by the lack of [3H]-acetylcholine release following incubation with either the choline uptake inhibitor hemicholinium or the choline acetyltransferase inhibitor bromoacetylcholine. Rats treated neonatally with capsaicin or with spinal nerve ligation as adults showed a significantly decreased K+-stimulated release of [3H]-acetylcholine from dorsal horn but not ventral horn lumbar spinal cord slices. In rats subjected to dorsal rhizotomy, while basal release from lumbar dorsal spinal cord slices was reduced, K+-stimulated [3H]-acetylcholine release, while decreased, was not significantly different compared with controls. The data presented here show that there are regional differences in the release of acetylcholine from spinal cord and that this release can be modulated by chemical or surgical deafferentation. These results also indicate that the source of acetylcholine in the dorsal cord originates mainly from resident somata and their collaterals, interneurons and/or descending terminals, with only very minor contributions coming from primary afferents. The present data help to further elucidate the role of acetylcholine in spinal signaling, particularly with respect to the effects of nerve injury and nociceptive neurotransmission.

Pharmacogenetic variability in neuronal nicotinic receptor-mediated antinociception.

The ability to predict interindividual differences in drug efficacy or toxicity, based on genetic factors that influence drug disposition or drug action, is fast becoming a realistic goal. The purpose of the present study was to determine whether epibatidine, a prototypical nicotinic analgesic drug, exhibits pharmacogenetic variability in antinociceptive activity. Eight inbred mouse strains (A, AKR, BALB/c, C3H/He, C57BL/6, C57BL/10, DBA/2, and SM) were surveyed for their sensitivity to the antinociceptive effects of epibatidine. All strains exhibited statistically significant antinociception that peaked between 10 and 20 min following the systemic injection of 50 microg/kg epibatidine. However, there was fourfold variability in the magnitude of peak effect between strains, with DBA/2, BALB/c and A strains showing much greater sensitivity than all others. A return to baseline nociceptive threshold at 30 min post-injection was observed for all but the A strain. In contrast, these mice exhibited significant antinociception for at least 3 h following epibatidine administration. Thus, expressing the data as area under the time-latency curve to take into account both the magnitude and duration of effect, epibatidine displayed approximately 20-fold higher antinociceptive potency in the A strain compared with the C3H/He strain. The effects of epibatidine in both the A and C3H/He strains were dose-dependent and sensitive to antagonism by the selective neuronal nicotinic channel blocker mecamylamine. Taken together, these data demonstrate the existence of pharmacogenetic variability in neuronal nicotinic receptor-mediated antinociception between inbred stains of mice and presage the potential for similar variability in analgesic response to nicotinic-based analgesics among humans. Future studies will seek to identify the chromosomal loci underlying this variability.

Antihyperalgesic activity of epibatidine in the formalin model of facial pain.

A growing body of evidence supports a nicotinic cholinergic approach to pain management, as neuronal nicotinic receptor agonists have shown efficacy across animal models of both inflammatory and neuropathic pain. However, most of these investigations have focused on the spinal system, and there is to date no report of nicotinic receptor-mediated antinociception in any pain model involving the trigeminal field of innervation. Thus, the purpose of the present studies was to evaluate whether the neuronal nicotinic receptor agonist epibatidine possesses antihyperalgesic activity in the formalin model of facial pain. Adult, male, Sprague--Dawley rats received a 50-microl, subcutaneous injection of 5% formalin into one vibrissal pad and the consequent, facial grooming behavior was monitored. Consistent with previous investigations using the formalin model, animals exhibited two periods of nocifensive grooming: (1) an acute phase that began immediately, peaked at 3 min and almost completely abated by 6 min, and (2) a tonic phase that began between 6 and 9 min, peaked at 21 min and slowly diminished over the ensuing 24 min. The subcutaneous administration of epibatidine (1--5 microg/kg) 5 min prior to the formalin injection led to a significant, dose-dependent reduction of both the acute and tonic phases of hyperalgesia. Separate groups of animals receiving epibatidine either 15, 30 or 60 min prior to the formalin injection exhibited a progressively diminishing antihyperalgesic response that was no longer significant in either phase by 30 min. Finally, pretreatment with the selective neuronal nicotinic receptor antagonist mecamylamine completely abolished the antihyperalgesic effect of epibatidine in both phases. Taken together, these studies demonstrate that in both the acute and tonic phases of the formalin model of facial pain, epibatidine produces a neuronal nicotinic receptor-mediated antihyperalgesia that is both dose- and time-dependent. These results support the rationale for exploring the clinical efficacy of nicotinic agonists as analgesics to treat certain types of trigeminal pain in humans.

Naltrexone blocks nicotine-induced prolactin release.

Two receptor populations involved in the release of prolactin were examined in conscious, freely moving, male rats bearing indwelling jugular cannulae. The intravenous administration of either nicotine or morphine increased plasma prolactin levels. Pretreatment with the nicotinic antagonist mecamylamine blocked the prolactin response to nicotine only. In contrast, the opiate antagonist naltrexone blocked the prolactin response to both nicotine and morphine. These findings indicate that the nicotine stimulated release of prolactin is dependent not only on functional nicotinic cholinergic receptors but on opiate receptors as well. This suggests that nicotine and morphine release prolactin via a common pathway containing nicotinic cholinergic and opiate synapses in series.

A comparison of multiple injections versus continuous infusion of nicotine for producing up-regulation of neuronal [3H]-epibatidine binding sites.

Chronic nicotine exposure in the rat produces a characteristic increase in neuronal nicotinic binding sites in many brain regions. The conventional method for inducing such increases utilizes twice daily subcutaneous injections of a near maximal, sub-convulsive dose of nicotine. Alternatively, nicotine may be chronically infused via an osmotic mini-pump. However, little is known about how administration of nicotine by chronic infusion compares to multiple injections in producing nicotinic receptor upregulation. This study used [3H]-epibatidine, a high potency neuronal nicotinic agonist radioligand, to compare the increases in receptor levels in rat brain, spinal cord and trigeminal ganglion tissues following chronic nicotine administration via either twice daily injections (2 mg/kg s.c.) or an osmotic mini-pump (1 mg/kg/hr) for 10 days. All central and peripheral nervous system tissues examined demonstrated significant neuronal nicotinic receptor up-regulation following chronic infusion of nicotine. Only the cerebral cortex and hippocampus displayed significant up-regulation following nicotine administration by injections. Moreover, in all tissues studied, the receptor levels measured were significantly higher in the animals that received nicotine by chronic infusion compared with multiple injections. These data indicate that chronic infusion of nicotine is a convenient and efficacious alternative to multiple injections for producing neuronal nicotinic receptor up-regulation in both central and peripheral nervous tissues.

Stimulation of serotonin1A receptors increases release of prolactin in the rat.

The effect of serotonin1A receptor agonists on release of prolactin was examined in awake, freely-moving male rats in which a catheter in the jugular vein allowed samples of blood to be collected periodically after intravenous injection of the agonist. The serotonin1A receptor agonist, 8-hydroxy-2(di-n-propylamino) tetralin (8-OHDPAT) increased concentrations of prolactin in plasma rapidly and in a dose-related manner. Concentrations of prolactin peaked within 9 min after intravenous injection of 8-OHDPAT and returned to baseline values within 30 min. Another serotonin1A receptor agonist, 5-methylurapidil (5-MeU), produced a similar response of prolactin. The effects of these agonists on release of prolactin were completely blocked by pretreatment with the serotonin receptor antagonists, methysergide and metergoline, administered 1 or 2 hr before the agonist. These results demonstrated that serotonin1A receptors can mediate the effects of serotonin on release of prolactin in the male rat.

Restraint stress-induced elevations in plasma corticosterone and beta-endorphin are not accompanied by alterations in immune function.

A variety of stressors activate the hypothalamic-pituitary-adrenal (HPA) axis, thereby resulting in elevated levels of circulating ACTH, beta-endorphin and corticosterone. Since these hormones have been shown previously to alter measures of immune function, we determined whether presentation of a stressor which activates the HPA axis produces a concomitant alteration in immune function. Restraint stress resulted in significantly elevated levels of corticosterone and beta-endorphin without affecting either proliferative or cytolytic activities of lymphocytes. At concentrations similar to those achieved during stress, in vivo, corticosterone exhibited a dose- and time-dependent reduction in both lymphocyte proliferation as well as natural killer cytotoxicity, in vitro. beta-Endorphin, on the other hand, was without direct or modulatory effects. These results indicate that restraint stress-induced activation of the HPA axis occurs without accompanying alterations in immune function.

Neuropeptide Y inhibits capsaicin-sensitive nociceptors via a Y1-receptor-mediated mechanism.

Neuropeptide Y (NPY) is expressed in certain primary afferent fibers, is up-regulated in response to tissue injury and is capable of inhibiting nociceptive behavior at the spinal level. However, the spinal mechanism(s) for NPY-evoked antinociception is unknown. In this study, we evaluated the hypothesis that agonists at the NPY Y1 receptor subtype (Y1-R) inhibit exocytosis from the capsaicin-sensitive class of nociceptors. Using in vitro superfusion of rat dorsal spinal cord slices, pre-treatment with the Y1-R agonist [Leu(31)Pro(34)]NPY significantly inhibited capsaicin-evoked release of immunoreactive calcitonin gene-related peptide with an EC(50) value of 10.6 nM. This inhibitory effect was concentration dependent, significantly attenuated by pre-treatment with the Y1 receptor antagonist BIBP3226 and reproduced by synthetic NPY. Examination of adult rat dorsal root ganglia using double immunofluorescent labeling revealed frequent co-localization of Y1 receptor immunoreactivity in vanilloid receptor type 1-immunoreactive neurons, indicating that Y1 agonists may directly modulate the capsaicin-sensitive class of nociceptors. Collectively, these results indicate that NPY is capable of inhibiting capsaicin-sensitive neurons via a Y1 receptor mechanism, suggesting the mechanisms for spinal NPY-induced antinociception is due, at least in part, to inhibition of central terminals of capsaicin-sensitive nociceptors.

The neuronal distribution of cannabinoid receptor type 1 in the trigeminal ganglion of the rat.

Cannabinoid compounds have been shown to produce antinociception and antihyperalgesia by acting upon cannabinoid receptors located in both the CNS and the periphery. A potential mechanism by which cannabinoids could inhibit nociception in the periphery is the activation of cannabinoid receptors located on one or more classes of primary nociceptive neurons. To address this hypothesis, we evaluated the neuronal distribution of cannabinoid receptor type 1 (CB1) in the trigeminal ganglion (TG) of the adult rat through combined in situ hybridization (ISH) and immunohistochemistry (IHC). CB1 receptor mRNA was localized mainly to medium and large diameter neurons of the maxillary and mandibular branches of the TG. Consistent with this distribution, in a de facto nociceptive sensory neuron population that exhibited vanilloid receptor type 1 immunoreactivity, colocalization with CB1 mRNA was also sparse (<5%). Furthermore, very few neurons (approximately 5%) in the peptidergic (defined as calcitonin gene-related peptide- or substance P-immunoreactive) or the isolectin B4-binding sensory neuron populations contained CB1 mRNA. In contrast, and consistent with the neuron-size distribution for CB1, nearly 75% of CB1-positive neurons exhibited N52-immunoreactivity, a marker of myelinated axons. These results indicate that in the rat TG, CB1 receptors are expressed predominantly in neurons that are not thought to subserve nociceptive neurotransmission in the noninjured animal. Taken together with the absence of an above background in situ signal for CB2 mRNA in TG neurons, these findings suggest that the peripherally mediated antinociceptive effects of cannabinoids may involve either as yet unidentified receptors or interaction with afferent neuron populations that normally subserve non-nociceptive functions.

The pharmacogenetics of analgesia: toward a genetically-based approach to pain management.

Interindividual differences in the experience of pain have been appreciated clinically for over a century. More recently, there has been a growing body of evidence demonstrating differences in analgesic response to various pharmacotherapies, although the source of this variability largely remains to be explained. To this end, basic science research is beginning to identify the allelic variants that underlie such antinociceptive variability using a multiplicity of animal models, and powerful genetic approaches are being exploited to accelerate this process. Although the vast majority of these studies have focused on the pharmacogenetics of opioids, owing to their prominent status as analgesics, the number of pharmacotherapies evincing genetically-based variability is rapidly expanding. In addition, analogous studies have been undertaken in humans, as a small but growing number of clinical trials have begun to evaluate prospectively the existence, if oftentimes not the origin, of interindividual differences in analgesic drug response. Importantly, with a few notable exceptions, such efforts have primarily identified differences in analgesic efficacy and/or potency between male and female human subjects. Looking toward the future development of one or more widely utilised, pharmacogenetic screens that would lead to modifications in treatment planning, at least with respect to the pharmacologic management of pain, this review will document the breadth of genetically-based variability in drug-mediated antinociception in animals. Specific examples in which the gene or genes underlying such variability have been postulated or identified will be given, while highlighting the effect of sex and its interactions with other genetic backgrounds. Finally, we will summarise and evaluate the literature on pharmacogenetic differences in human analgesic drug response, for which the influence of sex has served as one of the better studied and heuristically insightful examples.

Met5-enkephalin-Arg6-Gly7-Leu8 immunoreactivity in rat and human cerebrospinal fluid: influence of neuroleptic drugs and electroconvulsive shock.

Met5-Enkephalin-Arg6-Gly7-Leu8 immunoreactivity was quantitated in both rat and human cerebrospinal fluid (CSF) by radioimmunoassay with a carboxy-terminal directed antiserum. The immunoreactivity in CSF was chromatographically characterized in both species and was found to consist almost exclusively of high molecular weight forms. In human CSF there was approximately 300 fmol/ml and in the rat 1,500 fmol/ml of immunoreactivity. The possibility of a rostro-caudal gradient was examined in the human by analyzing the first and the twenty-fifth ml of CSF drawn during a lumbar puncture: none was found. The immunoreactivity was fairly stable; no loss of immunoreactivity was observed after 24 h of incubation of rat CSF at 37 degrees C. Electroconvulsive shock (ECS) produced a significant elevation in CSF content but only after a course of chronic administration; a single acute ECS produced no increase. Human subjects with schizophrenia who were being treated with antipsychotic drugs had elevated levels of immunoreactivity in comparison to non-mediated patients and normals. The high levels of this immunoreactivity in CSF, its stability and the evidence that the content can change with physiological and pharmacological manipulation indicate that Met5-Enkephalin-Arg6-Gly7-Leu8 immunoreactivity can serve as a new and useful CSF marker for investigating the CNS enkephalin system in neurological or psychiatric disorders.

beta 2-Adrenoceptor regulation of CGRP release from capsaicin-sensitive neurons.

Previous studies have suggested that neurotransmitter substances from the sympatho-adrenomedullary system regulate pulpal blood flow (PBF), in part, by the inhibition of vasoactive neuropeptide release from pulpal sensory neurons. However, no study has evaluated the role of beta-adrenoceptors. We evaluated the hypothesis that activation of beta-adrenoceptors inhibits immunoreactive calcitonin gene-related peptide (iCGRP) release from capsaicin-sensitive nociceptive neurons via in vitro superfusion of bovine dental pulp. Either norepinephrine or epinephrine inhibited capsaicin-evoked iCGRP. The norepinephrine effect was blocked by the selective beta(2)-adrenoceptor antagonist, ICI 118,551, but not by pre-treatment with the selective beta(1)-adrenoceptor antagonist, atenolol. In addition, application of albuterol, a selective beta(2)-adrenoceptor agonist, significantly blocked capsaicin-evoked release of iCGRP. Collectively, these studies demonstrate that activation of beta(2)-adrenoceptors in dental pulp significantly reduces exocytosis of neuropeptides from capsaicin-sensitive nociceptors. This effect may have physiologic significance in regulating PBF. Moreover, since capsaicin selectively activates nociceptors, beta(2)-adrenoceptor agonists may have clinical utility as peripherally acting therapeutics for dental pain and inflammation.

Modeling and experimental comparison of the differential adsorption of B1 and G1 aflatoxins on mineral aluminosilicate surfaces.

Aflatoxins produced by Aspergillus fungus are secondary metabolites undergoing biotransformation rates in hepatic tissues and lipid peroxidation. Although the use of adsorbent materials became a common practice for feed grain detoxification, fundamental studies are needed to clarify the interaction occurring between mineral surfaces and organic molecules. We evaluated the differential adsorption of B1 and G1 on 10 adsorbent materials and compared it in vitro by means of fluorescence emission from solution. Three aluminosilicates showed no adsorption of B1 at all, whereas only one was inactive for G1 adsorption and seven of them showed 15.2 to 77.9% adsorption for B1 and 8.3 to 78% for G1. All these adsorbents were more selective toward G1 rather than B1 aflatoxins. This behavior can be explained by the presence of an additional cyclic ester in G1, which provides a higher electronic density to G1 molecules, thus forming more stable hydrogen bridges with respect to the cyclopentanone ring present in B1.

An in vitro evaluation of the accuracy of the root ZX in the presence of various irrigants.

The purpose of this study was to evaluate the accuracy of the Root ZX in vitro in the presence of a variety of endodontic irrigants. The in vitro model, described by Donnelly, consisted of refrigerated gelatin made with 0.9% sodium chloride instead of water. The following irrigants were tested: 2% lidocaine with 1:100,000 epinephrine, 5.25% sodium hypochlorite, RC Prep, liquid EDTA, 3% hydrogen peroxide, and Peridex. A total of 30 extracted, single-rooted teeth were used. The experimental measurements in the presence of the various irrigants were compared with the actual canal lengths. The present data indicate that the Root ZX electronic apex locator reliably measured canal lengths to within 0.31 mm and that there was virtually no difference in the length determination as a function of the seven irrigants used. These results strongly support the concept that the Root ZX is a useful, versatile, and accurate device for the determination of canal lengths over a wide range of irrigants commonly used in the practice of endodontics.

Epidemiological evaluation of the outcomes of nonsurgical root canal treatment in a large cohort of insured dental patients.

Selected outcomes following initial nonsurgical root canal treatment (NSRCT) procedures were retrospectively assessed using an insurance company database of 110,766 nonsurgical root canal procedures that were completed by endodontists and their referring general dentists. A subset of 44,613 cases, with a minimum required follow-up time of 2 yr, showed incidences of extraction, retreatment and periradicular surgery equal to 5.56%, 2.47%, and 1.41%, respectively. The incidence of subsequent extraction increased with patient age. Teeth that were not restored after root canal therapy were significantly more likely to undergo extraction than restored teeth. Although the practice pattern for endodontists consisted of a significantly higher proportion of molars (48% more; p < 0.001) and a smaller proportion of anterior teeth (43% less; p < 0.001) than general dentists, both groups of providers had comparable rates of untoward events. These data strongly support the hypothesis that the specialist practice provides similar rates of clinical success compared with other providers, even when treating significantly more complex NSRCT cases. Overall, 94.44% of nonsurgical root canal treated teeth remained functional over an average follow-up time of 3.5 yr. These results are an important indication of the benefits of endodontic treatment when provided in an integrated health care delivery system of endodontists and their referring general dentists.