Biomedical subjects

J M Carter

Publications and source records attributed to J M Carter.

At least 37 records · Page 2Linked to original sources

PubMed1999

U18666A inhibits intracellular cholesterol transport and neurotransmitter release in human neuroblastoma cells.

To determine if neurochemical function might be impaired in cell models with altered cholesterol balance, we studied the effects of U18666A (3-beta-[(2-diethyl-amino)ethoxy]androst-5-en-17-one) on intracellular cholesterol metabolism in three human neuroblastoma cell lines (SK-N-SH, SK-N-MC, and SH-SY5Y). U18666A (< or =0.2 microg/ml) completely inhibited low density lipoprotein (LDL)-stimulated cholesterol esterification in SK-N-SH cells, while cholesterol esterification stimulated by 25-hydroxycholesterol or bacterial sphingomyelinase was unaffected or partially inhibited, respectively. U18666A also blocked LDL-stimulated downregulation of LDL receptor and caused lysosomal accumulation of cholesterol as measured by filipin staining. U18666A treatment for 18 h resulted in 70% inhibition of K+-evoked norepinephrine release in phorbol ester-differentiated SH-SY5Y cells, while release stimulated by the calcium ionophore A23187 was only slightly affected. These results suggest that U 18666A may preferentially block a voltage-regulated Ca2+ channel involved in norepinephrine release and that alterations in neurotransmitter secretion might be a feature of disorders such as Niemann-Pick Type C, in which intracellular cholesterol transport and distribution are impaired.

Androstenes↗

PubMed1999

The eye lens cytoskeleton.

During lens cell differentiation there are a number of very characteristic morphological changes that occur. These include a 50- to 100-fold increase in cell length as the equatorial lens epithelial cells differentiate into fibre cells and the loss of the cellular organelles such as mitochondria, nuclei, Golgi apparatus and endoplasmic reticulum. Coincident with these changes are dramatic alterations in the organisation of the lens fibre cell cytoskeleton and in particular the lens-specific intermediate filament network comprising CP49 and filensin. Cell shape and cell polarisation as well as tissue integrity are all processes that depend upon the cytoskeleton and are therefore important to the lens. The unique aspects of the lenticular cytoskeleton are the subject of this review.

Animals↗

PubMed1999

Feasibility of finding an unrelated bone marrow donor on international registries for New Zealand patients.

Allogeneic bone marrow transplantation is the treatment of choice for several hematological conditions. Unfortunately, for the majority (70%) of patients an HLA-matched sibling donor is not available and a matched unrelated donor must be found if they are to proceed to allogeneic transplantation. Most of the donors on international registries are of Caucasian ethnic origin. It has been recognized that patients from certain racial groups have a reduced chance of finding an unrelated donor. This study reports the feasibility of finding an unrelated donor for our local New Zealand patients of Caucasian, New Zealand Maori and Pacific Islander ethnic origin presenting with transplantable hematological conditions at a single center. The search was performed on international registries using HLA-A,B and DR typings for our patients. Six of six and five of six matches were evaluated. We have shown that Maori and Pacific Islanders have significantly lower hit rates than Caucasians when searched for 6/6 antigen matches, but there was no significant difference between the three ethnic groups in finding a 5/6 antigen matched donor. This study supports the policy of the New Zealand Bone Marrow Donor Registry in recruiting New Zealand Maori and Pacific Islanders.

Bone Marrow Transplantation↗

PubMed1999

Effect of Sch 55700, a humanized monoclonal antibody to human interleukin-5, on eosinophilic responses and bronchial hyperreactivity.

This report describes the development and the biology of Sch 55700, a humanized monoclonal antibody to human IL-5 (hIL-5). Sch 55700 was synthesized using CDR (complementarity determining regions) grafting technology by incorporating the antigen recognition sites for hIL-5 onto consensus regions of a human IgG4 framework. In vitro, Sch 55700 displays high affinity (Kd = 20 pmol/l) binding to hIL-5, inhibits the binding of hIL-5 to Ba/F3 cells (IC50 = 0.5 nmol/l) and blocks IL-5 mediated proliferation of human erythroleukemic TF-1 cells. In allergic mice, Sch 55700 (0.1-10 mg/kg, i.p. or i.m.) inhibits the influx of eosinophils in the lungs, demonstrates long duration of activity and the anti-inflammatory activity of this compound is additive with oral prednisolone. In allergic guinea pigs, Sch 55700 (0.03-30 mg/kg i.p.) inhibits both the pulmonary eosinophilia and airway hyperresponsiveness and at 30 mg/kg, i.p. inhibited allergic, but not histamine-induced bronchoconstriction. In allergic rabbits, Sch 55700 blocks cutaneous eosinophilia. Sch 55700 (0.1-1 mg/kg i.p.) also blocks the pulmonary eosinophilia and neutrophilia caused by tracheal injection of hIL-5 in guinea pigs. In allergic cynomolgus monkeys, a single dose of Sch 55700 (0.3 mg/kg i.v.) blocks the pulmonary eosinophilia caused by antigen challenge for up to six months. Sch 55700 is, therefore, a potent antibody against IL-5 in vitro and in a variety of species in vivo that could be used to establish the role of IL-5 in human eosinophilic diseases such as asthma.

Animals↗

PubMed1999

Clubfoot analysis with three-dimensional foot models.

The purpose of this study was to develop a method of defining, in mathematical terms, the interpositional relationships of the bones of the hindfoot complex in the idiopathic clubfoot and the neurogenic clubfoot. The neurogenic clubfoot and contralateral normal-appearing foot of a stillborn infant with myelomeningocele, and the normal foot of a 10-year-old were sectioned with a cryomicrotome. Magnetic resonance images (MRIs) of the clubfoot and the normal foot of a 3-month-old boy were obtained. Using a computer program, three-dimensional foot models were generated from the digitized cryomicrotome sections and from the MRIs. The central principal axes were determined for the talus and calcaneus. The long central principal axes of the talus and calcaneus were neutrally rotated with reference to the bimalleolar axis in the idiopathic clubfoot while in the neurogenic clubfoot the long central principal axis of the talus was medially rotated 52 degrees and that of the calcaneus 10 degrees. The talocalcaneal angles defined by the long central principal axes in the superior and medial views were 0 degree and 10 degrees, respectively, in the idiopathic clubfoot, and 42 degrees and 56 degrees, respectively, in the neurogenic clubfoot.

Biomechanical Phenomena↗

PubMed1998

Analysis of thermal stability of soya globulins using monoclonal antibodies.

The epitopes of two monoclonal antibodies (Mabs), one raised to soya glycinin (IFRN 0025) and one to beta-conglycinin (IFRN 0089), have been defined. The epitope of 0025 corresponds to residues 86-104 of the acidic polypeptide of glycinin A1aB1b and lies at the C terminus of the proteolytic intermediate known as glycinin-T, whilst that of 0089 corresponds to residues 78-84 in the acidic extension present in the alpha' subunit of beta-conglycinin. As the Mabs bind to synthetic peptides corresponding to the epitope regions both epitopes can be considered as being continuous in nature. The regions recognised correspond to surface loops, which are probably flexible in nature. Both Mabs were used to investigate thermally induced conformational changes in soya globulins. Thermally treated glycinin was recognised more strongly than native protein, possibly due to disruption of the disulphide bond joining the acidic and basic polypeptides. Disruption could increase epitope accessibility, as could the conformational changes associated with denaturation. The binding of anti-beta-conglycinin Mab 0089 was unaffected by heating, suggesting that its epitope remains on the surface of the aggregates formed on heating. This study demonstrates that Mabs with defined specificities can be sensitive probes for monitoring local conformational changes within a protein molecule during thermal denaturation.

Amino Acid Sequence↗

PubMed1998

Regulated spacing of synapses and presynaptic active zones at larval neuromuscular junctions in different genotypes of the flies Drosophila and Sarcophaga.

Synapses at larval neuromuscular junctions of the flies Drosophila melanogaster and Sarcophaga bullata are not distributed randomly. They have been studied in serial electron micrographs of two identified axons (axons 1 and 2) that innervate ventral longitudinal muscles 6 and 7 of the larval body wall. The following fly larvae were examined: axon 1--wild-type Sarcophaga and Drosophila and Drosophila mutants dunce(m14) and fasII(e76), a hypomorphic allele of the fasciclin II gene; and axon 2--drosophila wild-type, dunce(m14), and fasII(e76). These lines were selected to provide a wide range of nerve terminal phenotypes in which to study the distribution and spacing of synapses. Each terminal varicosity is applied closely to the underlying subsynaptic reticulum of the muscle fiber and has 15-40 synapses. Each synapse usually bears one or more active zones, characterized by dense bodies that are T-shaped in cross section; they are located at the presumed sites of transmitter release. The distribution of synapses was characterized from the center-to-center distance of each synapse to its nearest neighbor. The mean spacing between nearest-neighbor pairs ranged from 0.84 microm to 1.05 microm for axon 1, showing no significant difference regardless of genotype. The corresponding values for axon 2, 0.58 microm to 0.75 microm, were also statistically indistinguishable from one another in terminals of different genotype but differed significantly from the values for axon 1. Thus, the functional class of the axon provides a clear prediction of the spacing of its synapses, suggesting that spacing may be determined by the functional properties of transmission at the two types of terminals. Individual dense bodies were situated mostly at least 0.4 microm away from one another, suggesting that an interaction between neighboring active zones could prevent their final positions from being located more closely.

Animals↗

PubMed1998

Interleukin-10 regulates quartz-induced pulmonary inflammation in rats.

Interleukin-10 (IL-10) can downregulate expression of several proinflammatory cytokines including chemokines. This study investigated the role of IL-10 in the acute response of the rat lung to quartz particles. Intratracheal instillation of rats with 1 mg of quartz produced an inflammatory and cytotoxic response demonstrated by increased bronchoalveolar lavage (BAL) fluid neutrophils, lactate dehydrogenase, and protein. IL-10 was detected in rat lung, but IL-10 levels were not altered by quartz. In contrast, quartz increased lung levels of the chemokine macrophage inflammatory protein-2 (MIP-2). Treatment with recombinant murine IL-10 (rmIL-10) attenuated quartz-induced pulmonary inflammation and injury. Pretreatment with anti-IL-10 antiserum enhanced inflammatory responses to quartz. Consistent with effects on quartz-induced inflammation, rmIL-10 and anti-IL-10 serum decreased and increased, respectively, lung MIP-2 mRNA and protein in response to quartz. Additionally, rmIL-10 reduced production of hydrogen peroxide, superoxide anion, and nitric oxide by BAL cells from quartz-exposed and control rats. These results demonstrate that IL-10 is expressed in rat lung and downregulates quartz-induced inflammation and cell activation. The mechanism of the anti-inflammatory action of IL-10 after quartz administration involves, at least in part, attenuation of MIP-2 expression.

Animals↗

PubMed1998

Crocidolite activates NF-kappa B and MIP-2 gene expression in rat alveolar epithelial cells. Role of mitochondrial-derived oxidants.

Nuclear factor kappa B (NF-kappa B) is a transcription factor that regulates expression of several genes coding for inflammatory and immunoregulatory proteins including the neutrophil chemotactic cytokine MIP-2. In previous studies we found that crocidolite asbestos activates the nuclear translocation of NF-kappa B as well as MIP-2 gene expression in rat alveolar type II cells. Here we report that both crocidolite-induced NF-kappa B activation of MIP-2 gene expression can be attenuated by the antioxidant tetramethylthiourea, suggesting the dependence of these responses on oxidative stress. Crocidolite exposure of RLE-TN cells also increased production of H2O2, a response that was inhibited by the mitochondrial respiratory chain inhibitor thenoyltrifluoroacetone (TTFA). TTFA treatment of RLE-6TN cells also inhibited crocidolite-induced nuclear translocation of NF-kappa B and MIP-2 gene expression. These results indicate crocidolite exposure of rat alveolar type II cells results in increased production of mitochondrial-derived hydrogen peroxide and that mitochondrial-derived oxidants contribute to crocidolite activation of NF-kappa B and increases in MIP-2 gene expression.

Animals↗

PubMed1997

Merozoite surface protein-1 epitopes recognized by antibodies that inhibit Plasmodium falciparum merozoite dispersal.

Serum antibodies from malaria immune donors can inhibit merozoite dispersal by forming immune complexes through surface-accessible regions of membrane associated antigens. Such merozoite forms are referred to as immune clusters of merozoites (ICM). Antibodies dissociated from ICM of Plasmodium falciparum identify a restricted subset of antigens, including merozoite surface protein-1 (MSP-1). We performed epitope mapping by comparing the reactivity of whole immune sera and ICM-derived antibodies in immunoblotting assays, using fourteen overlapping recombinant MSP-1 fragments, and by ELISA, using each of the 1720 octapeptides encoded within MSP-1. Antibodies in immune sera reacted with thirteen recombinant fragments and hundreds of octapeptides, but antibodies derived from ICM reacted with only six recombinant fragments and twenty octapeptides. Recombinant fragment recognition by ICM-derived antibodies was delimited to three regions 150-200 residues long, with seven of the octapeptide epitopes also mapping to these regions. The octapeptides recognized most strongly by antibodies in whole serum corresponded to the degenerate repeats near the N-terminus of MSP-1, however, neither recombinant fragments, nor octapeptides containing these degenerate repeats, were recognized by ICM-derived antibodies. Compared to reactions with recombinant fragments, the reactions observed with octapeptides were weak and may represent low-affinity mimetopes or cross-reactions. Alternatively, they may represent reactions with a portion of an epitope assembled from more than one non-contiguous peptide. These results suggest that ICM-derived antibodies can be used to map surface-accessible epitopes on MSP-1 and that the recombinant fragments with which they react are appropriate candidates for further evaluation as components of a malaria vaccine.

Animals↗

PubMed1997

Identification of novel human WW domain-containing proteins by cloning of ligand targets.

A recently described protein module consisting of 35-40 semiconserved residues, termed the WW domain, has been identified in a number of diverse proteins including dystrophin and Yes-associated protein (YAP). Two putative ligands of YAP, termed WBP-1 and WBP-2, have been found previously to contain several short peptide regions consisting of PPPPY residues (PY motif) that mediate binding to the WW domain of YAP. Although the function(s) of the WW domain remain to be elucidated, these observations strongly support a role for the WW domain in protein-protein interactions. Here we report the isolation of three novel human cDNAs encoding a total of nine WW domains, using a newly developed approach termed COLT (cloning of ligand targets), in which the rapid cloning of modular protein domains is accomplished by screening cDNA expression libraries with specific peptide ligands. Two of the new genes identified appear to be members of a family of proteins, including Rsp5 and Nedd-4, which have ubiquitin-protein ligase activity. In addition, we demonstrate that peptides corresponding to PY and PY-like motifs present in several known signaling or regulatory proteins, including RasGAP, AP-2, p53BP-2 (p53-binding protein-2), interleukin-6 receptor-alpha, chloride channel CLCN5, and epithelial sodium channel ENaC, can selectively bind to certain of these novel WW domains.

Amino Acid Sequence↗

PubMed1997

Effects of particle exposure and particle-elicited inflammatory cells on mutation in rat alveolar epithelial cells.

To investigate mechanisms underlying development of lung adenomas and carcinomas in rats exposed to poorly soluble particles the relationships between particle exposure, inflammation and mutagenesis in rat alveolar type II cells were characterized. Rats were exposed to saline or saline suspensions of 10 and 100 mg/kg of alpha-quartz, carbon black or titanium dioxide by intratracheal instillation. Fifteen months after exposure, bronchoalveolar lavage (BAL) cells were characterized as to number and type and lung histopathology performed. The alveolar type II cells were isolated and cultured in 6 thioguanine (6TG) containing media to select for mutation in the hprt gene. The potential contribution of lung inflammatory cells to in vivo mutagenic responses, were evaluated by co-culturing BAL cells with the rat alveolar epithelial cell line, RLE-6TN for 24 h and the RLE-6TN cells selected for 6TG resistance. Neutrophilic inflammation was detected in all rats exposed to 10 and 100 mg/kg of alpha-quartz and carbon black and 100 mg/kg titanium dioxide; epithelial hyperplasia was observed in rats exposed to 10 and 100 mg/kg of alpha-quartz and 100 mg/kg carbon black. Hprt mutation frequency was increased in alveolar type II cells from rats exposed to 10 and 100 mg/kg of alpha-quartz, 100 mg/kg carbon black and 100 mg/kg titanium dioxide. In vitro exposure of RLE-6TN cells to BAL cells from rats treated with 10 and 100 mg/kg of alpha-quartz or 100 mg/kg carbon black increased hprt mutant frequency. Both macrophage and neutrophil enriched BAL cell populations were mutagenic to RLE-6TN cells, however, the mutagenic activity appeared greatest for neutrophils. Addition of catalase to BAL cell:RLE-6TN co-cultures inhibited the increase in hprt mutation frequency. These studies demonstrate exposure of rats to doses of particles producing significant neutrophilic inflammation is associated with increased mutation in rat alveolar type II cells. The ability of particle-elicited macrophages and neutrophils to exert a mutagenic effect on epithelial cells in vitro supports a role for these inflammatory cells in the in vivo mutagenic effects of particle exposure. The inhibition of BAL cell-induced mutations by catalase implies a role for cell-derived oxidants in this response.

Animals↗

PubMed1997

A qualitative and quantitative analysis of the entorhinal cortex in schizophrenia.

The entorhinal cortex (ERC) has been implicated in schizophrenia by a number of studies. There is anatomical observation of neuronal heterotopias in the rostral ERC, which is consistent with a hypothesis of neurodevelopmental abnormalities in this disease. In view of the significant cytoarchitectonic variation of the ERC throughout its rostro-caudal extent, we performed a detailed subareal analysis of the rostral two-thirds of the entorhinal cortex (ERCr) in 14 postmortem schizophrenic brains and 14 matched controls (mean ages of 48 and 47 respectively). This systematic evaluation included both a qualitative microscopic analysis of morphogenetic anomalies that would be consistent with neurodevelopmental pathology and quantitative measurements of total neuronal number, average neuronal density, laminar volume and laminar depth from the cortical surface in cytoarchitectonically matched subareas of schizophrenic and control brains. Parcellation of the entire ERC on the basis of cytoarchitectonic criteria identified five distinct regions, similar to those described in the macaque, except that in the human brain three of the regions were further divisible into two or three subareas, yielding nine distinct cellular compartments. Five rostral areas, prorhinal (Pr), lateral (28L), intermediate rostral and caudal (281r and 281c), and sulcal (28S), comprise the ERCr. Gross and microscopic examination of these subdivisions throughout the ERCr failed to reveal laminar disorganization in any of the schizophrenic brains. The brains also did not differ significantly with respect to total neuronal number, total volume and neuronal density per laminar and subareal subdivision, or laminar thickness per entorhinal subarea. However, neuronal number and density were reduced by 12-18% in Pr and 28L, suggesting that mild quantitative abnormalities may exist in the ERCr and might possibly be revealed in a larger sample of schizophrenic brains. We have failed to confirm previous reports of laminar disorganization in the ERCr in brains of patients with schizophrenia; to the extent that this region is implicated in schizophrenia, the structural changes are likely to consist of more subtle cellular disturbances.

Adult↗

PubMed1997

Cytokines and particle-induced inflammatory cell recruitment.

The inflammatory response is a key component of host defense. However, excessive or persistent inflammation can contribute to the pathogenesis of disease. Inflammation is regulated, in part, by cytokines, which are small, typically glycosylated proteins that interact with membrane receptors to regulate cellular processes such as proliferation, differentiation, and secretion. During the past 10 years studies in humans and experimental animals have demonstrated that a cytokine called tumor necrosis factor alpha (TNF-alpha) plays a key role in the initiation of inflammatory responses in the lung and other tissues, including inflammation resulting from inhalation of noxious particles. There is now compelling evidence that one of the pathways by which inhaled particles stimulate the recruitment and subsequent activation of inflammatory cells is through the activation of lung macrophages to release TNF-alpha. TNF-alpha then acts via paracrine and autocrine pathways to stimulate cells to release other cytokines known as chemokines, which are directly chemotactic to leukocytes and other cells that participate in inflammatory and wound healing responses. In addition to a TNF-alpha-mediated pathway, there is growing evidence that some particles such as quartz and crocidolite can directly activate lung epithelial cells to release chemokines such as macrophage inflammatory protein-2, cytokine-induced neutrophil chemoattractant, and interleukin-8. A direct stimulatory effect of particles on lung epithelium may represent an additional or alternate pathway by which inhaled particles may elicit inflammation in the lung. Recent studies have suggested that oxidative stress may be a component of the mechanism by which particles activate cytokine production in cells such as macrophages and epithelial cells. The contribution of oxidative stress to particle-induced cytokine gene expression appears to be mediated, at least in part, through activation of the transcription factor nuclear factor kappa B.

Animals↗

PubMed1996

Multi-well ELISA based on independent peptide antigens for antibody capture. Application to Lyme disease serodiagnosis.

Novel procedures for the use of peptides as antibody-capture reagents in the ELISA format have been investigated. Epitope sequences from known immunodominant antigens of Borrelia burgdorferi were selected by screening peptide libraries with sera from patients with Lyme disease. Several epitope peptides were synthesized and immobilized, separately, on the ELISA plate as haptens on bovine serum albumin. Based on a comparative analysis of serum samples, it appears that peptide antigens can be used as effectively as a whole cell lysate to discriminate between Lyme disease and non-Lyme disease sera, thus avoiding dependence on bacterial sonicates which vary from passage to passage. Further improvements in epitope design for enhancement of accuracy in serodiagnosis are discussed.

Amino Acid Sequence↗

PubMed1996

Pulmonary inflammatory, chemokine, and mutagenic responses in rats after subchronic inhalation of carbon black.

Chronic inhalation of carbon black can produce carcinomas in rat lungs. At present the mechanisms underlying the rat lung tumor response to carbon black are unknown, although a significant role for inflammation and cell proliferation has been postulated. To investigate the processes which may contribute to development of rat lung tumors after carbon black exposure, we characterized the effects of subchronic inhalation of carbon black by rats on mutagenesis in alveolar epithelial cells, pulmonary inflammation, inflammatory cytokine/growth factor expression, and lung histopathology. Briefly, rats were exposed for 6 hr/day, 5 days/week for up to 13 weeks to 1.1, 7.1, and 52.8 mg/m3 carbon black and the effects on the lung were characterized after 6.5 and 13 weeks of exposure and 3 and 8 months of recovery. Endpoints characterized after carbon black exposure included mutation in the hprt gene of alveolar epithelial cells, changes in bronchoalveolar lavage fluid markers of lung injury and inflammation, expression of mRNA for the chemokines, MIP-2 and MCP-1, and lung histopathology. Lung burdens of carbon black were also determined. After 13 weeks of exposure to 1.1, 7.1, and 52.8 mg/m3 carbon black, lung burdens were 354, 1826, and 7861 micrograms carbon black, respectively. The lung clearance of carbon black appeared impaired after exposure to 7.1 and 52.8 mg/m3 carbon black, with the effects being more pronounced at the higher exposure level. Subchronic inhalation of 1.1 mg/m3 carbon black did not elicit any detectable adverse lung effects. A significant increase in hprt mutation frequency in alveolar epithelial cells was detected immediately after 13 weeks of exposure to 7.1 and 52.8 mg/m3 carbon black as well as after 3- and 8-month recovery periods for the group exposed to 52.8 mg/m3. No increase in hprt mutation frequency was observed for epithelial cells obtained from rats exposed to 1.1 mg/m3 carbon black. The observation that genotoxic effects (i.e., mutations) on alveolar epithelial cells occurred only after carbon black exposures which resulted in significant inflammation and epithelial hyperplasia supports the hypothesis that inflammatory cell-derives oxidants and increased cell proliferation play a role in the pathogenesis of rat lung tumors in response to carbon black.

Administration, Inhalation↗

PubMed1996

Binding properties of SH3 peptide ligands identified from phage-displayed random peptide libraries.

Combinatorial libraries have yielded high-affinity ligands for SH3 domains of a number of different proteins. We have shown that synthetic peptides containing these SH3 ligand sequences serve as specific probes of SH3 domains. Direct binding of the N-terminal biotinylated peptide ligands was conveniently detected in ELISA, filter-blotting, and dot-blotting experiments with the use of streptavidin-conjugated enzymes. In some cases, detection of peptide-SH3 interactions required that the biotinylated peptides first were preconjugated with streptavidin to form a multivalent complex. Interestingly, these nominally tetravalent SH3 peptide ligands cross-react to varying degrees with different SH3 domains. We have used such complexes to screen lambda cDNA expression libraries and have isolated clones that encode both known and novel SH3-domain-containing proteins. Based on the success of this methodology, we propose a general strategy by which ligands of a modular domain-containing protein can be isolated from random peptide libraries and used to screen cDNA expression libraries systematically for novel modular domain-containing proteins.

Amino Acid Sequence↗

PubMed1996

Transient effects of low-energy CO2 laser irradiation on dentinal impedance: implications for treatment of hypersensitive teeth.

This study evaluated the effect of CO2 laser irradiation on dentinal impedance by passing known cyclic potentials across dentinal wafers mounted as a window in an electrolytic cell and measuring the resulting electrical impedance. Wafers were equilibrated in 0.1 M of KCl. The wafer specimens were irradiated with a CO2 laser (12 W, 0.1 ms, energy density 1.25 J/cm2). The time for impedance equilibration after irradiation was compared with equilibration after mounting. Mounted samples required 48 h to approach equilibrium in the electrolyte. After laser irradiation, impedance of previously equilibrated samples also required 48 h to equilibrate. This, along with exponential curve fitting, confirmed that laser treatment reintroduced a transient alteration in impedance. Equilibration time after irradiation and the mounting were similar. Dentin desociation apparently caused this transient impedance. Energy dispersive X-ray analysis confirmed the disappearance of K+Cl- after irradiation. Therefore, laser irradiation may cause dentinal desociation, yielding temporary clinical relief of dentinal hypersensitivity until rehydration occurs.

Carbon Dioxide↗