Search PubMed⌕ Search

Biomedical subjects

Y Park

Publications and source records attributed to Y Park.

At least 109 records · Page 6Linked to original sources
PubMed2000

The effect of regular salbutamol on lung function and bronchial responsiveness in patients with primary ciliary dyskinesia.

STUDY OBJECTIVE: There is growing evidence that regular beta(2)-agonist use in patients with asthma is associated with decreased airway caliber and increased bronchial responsiveness. The aim of this study was to determine whether regular treatment with beta(2)-agonists induces changes in lung function and bronchial responsiveness in patients with primary ciliary dyskinesia. DESIGN: A randomized, double-blind, placebo-controlled, crossover study. PATIENTS: Nineteen children with primary ciliary dyskinesia. INTERVENTIONS: Subjects received inhaled salbutamol or identical placebo (2 x 100 microg qid) for periods of 6 weeks with a wash-out period of 4 weeks. MEASUREMENTS AND RESULTS: FEV(1) was measured before and 3 weeks and 6 weeks after salbutamol or placebo treatment. High-dose methacholine inhalation tests were performed before and 6 weeks after each treatment. The provocative concentration of methacholine producing a 20% fall in FEV(1) (PC(20)) and maximal airway narrowing (MDeltaFFEV(1)) was measured. No significant change in FEV(1) was observed during the salbutamol or placebo periods. No significant differences in the parameters of bronchial responsiveness (PC(20) and MDeltaFFEV(1)) were noted as the result of either salbutamol or placebo treatment. CONCLUSION: Our data have shown that salbutamol, inhaled regularly for 6 weeks, did not cause either a decline in lung function or an increase in bronchial responsiveness in subjects with primary ciliary dyskinesia.

Administration, Inhalation↗
PubMed2000

Effects of immobilization stress on estrogen-induced surges of luteinizing hormone and prolactin in ovariectomized rats.

Reproductive function has been known to be impaired by various kinds of physical and emotional stress, but the mechanism by which stress impairs the reproductive axis has not been clearly understood. In the present study, the effects of immobilization stress were studied on the surges of luteinizing hormone (LH) and prolactin (PRL) induced by 17beta-estradiol (E2) in ovariectomized rats. Two weeks after bilateral ovariectomy, animals were implanted with the capsule containing E2 or vehicle at 1000 h (designated as d 0). Immobilization was started at 1000 h and continued to 2100 h on d 2. Blood samples were collected according to the time schedule by a jugular vein catheter procedure. Immobilization stress inhibited basal release of LH and abolished E2-induced LH and PRL surges in ovariectomized (OVX) rats. Daily repeated immobilization (from 1200 h to 1800 h, 6 h/d) for 3 d also abolished LH and PRL surges when examined at 1800 h on d 2. Although daily repeated immobilization stress reduced E2-induced PRL mRNA levels, this stress failed to change LHbeta mRNA levels in the anterior pituitary as determined by Northern blot analysis. Gonadotropin-releasing hormone (GnRH) receptor mRNA levels in the anterior pituitary were lowered by immobilization stress in the OVX, E2-treated group. Dopamine D2 receptor mRNA levels in the anterior pituitary of OVX, E2-treated rats were significantly decreased at 1800 h, compared with those at 1000 h. However, immobilization prevented a decrease in dopamine D2 receptor mRNA levels at 1800 h. GnRH content was increased in the mediobasal hypothalamus by immobilization in the OVX, E2-treated group, suggesting that GnRH release was inhibited. Interestingly, GnRH mRNA levels in the preoptic area-anterior hypothalamic area were suppressed by immobilization stress in OVX, E2-treated rats when determined at 1800 h. Therefore, we concluded that immobilization stress blocks E2-induced LH surge possibly by inhibiting synthesis and release of GnRH at the hypothalamic level, and an increase of dopaminergic activity via D2 receptor at the pituitary level might be involved in the stress blockage of E2-induced PRL surge.

Animals↗
PubMed2000

Homologous upregulation of gonadotropin-releasing hormone receptor mRNA occurs through transcriptional activation rather than modulation of mRNA stability.

In a previous study, we showed that even continuous application of gonadotropin-releasing hormone (GnRH) could increase the steady-state levels of GnRH receptor (GnRH-R) mRNA if treated for a relatively short period (6 h). Therefore, in the present study we examined whether GnRH-induced increment of GnRH-R mRNA is owing to stabilization of the preexisting GnRH-R mRNA or new synthesis of GnRH-R mRNA or both. Initially, to examine the effect on new RNA synthesis, the transcription inhibitor, actinomycin D (2 microM), was added to primary cultured rat anterior pituitary cells. In the presence of transcription inhibitor, GnRH-induced augmentation of GnRH-R mRNA levels was completely abolished. This result indicates that homologous upregulation of GnRH-R mRNA expression occurs at least through new RNA synthesis of GnRH-R gene. We further assessed the effects of GnRH on the turnover rate of GnRH-R mRNA using actinomycin D (2 microM). The basal half-life of GnRH-R mRNA was estimated to be approx 21 h. The application of GnRH tended to slightly suppress the basal turnover rate of GnRH; however, there was no statistically significant difference, compared with the group treated with actinomycin D alone. Collectively, our results suggest that the homologous upregulation of GnRH-R mRNA may occur through transcriptional activation of GnRH-R gene rather than enhancement of GnRH-R mRNA stability, although we did not examine the transcription rate of GnRH-R gene.

Animals↗
PubMed2000

Progesterone together with estrogen attenuates homologous upregulation of gonadotropin-releasing hormone receptor mRNA in primary cultured rat pituitary cells.

In a previous study, we clearly demonstrated that an application of gonadotropin-releasing hormone (GnRH) to cultured rat pituitary cells increased the expression of GnRH receptor (GnRH-R) mRNA through transcriptional activation of GnRH-R gene rather than suppression of the turnover rate of GnRH-R mRNA. Along with GnRH, gonadal steroids seem to be an important regulator for GnRH-R expression in the pituitary gland. Recent in vivo studies reported that an application of gonadal steroids to gonadectomized animals modulated GnRH-R mRNA expression in the pituitary gland. However, it has not been clearly understood whether steroids may act directly at the pituitary or indirectly via modulation of hypothalamic GnRH release. Therefore, we assessed the effects of estrogen and progesterone on GnRH-R mRNA expression in primary cultured female rat pituitary cells. Neither estradiol nor progesterone modulates the basal expression of GnRH-R mRNA in primary cultured pituitary cells. When cultured pituitary cells were exposed to different doses of estradiol in combination with GnRH (0.2 nM), the GnRH-stimulated increment of GnRH-R mRNA expression was not significantly changed by estradiol at any given doses. However, when different doses of progesterone were added to primary cultured pituitary cells in combination with GnRH (0.2 nM), GnRH-induced increases in GnRH-R mRNA levels were reduced in a dose-related manner, showing a significant reduction at 100 nM progesterone. Furthermore, the addition of estradiol reinforced the suppressive effect of progesterone on the homologous upregulation of GnRH-R mRNA expression. Collectively, our results clearly demonstrated that progesterone directly attenuates the homologous upregulation of GnRH-R mRNA expression at the pituitary level, and that estradiol potentiates the effect of progesterone.

Animals↗
PubMed2000

Late abnormal findings on high-resolution computed tomography after Mycoplasma pneumonia.

BACKGROUND: The clinical course of Mycoplasma pneumonia is typically mild and self-limited. There are, however, several case reports of severe complication following this illness with considerable morbidity and mortality. OBJECTIVES: This study was conducted to investigate, using high-resolution computed tomography (HRCT), the long-term pulmonary structural abnormalities after Mycoplasma pneumonia and to identify risk factors (chest radiograph findings, antibody titers, and host factors) that might increase the likelihood of developing the sequelae. METHODS: Thirty-eight children requiring hospitalization attributable to Mycoplasma pneumonia were recruited by the retrospective examination of hospital records. They underwent HRCT after an interval of 1.0 to 2. 2 years. A control group of 17 children with the history of Mycoplasma upper respiratory infection was also studied after a similar interval. RESULTS: Abnormal HRCT findings were present in 37% (14/38) of the pneumonia group, compared with 12% (2/17) of the control group. The abnormalities in the pneumonia group, which appeared alone or in combination, included mosaic perfusion (n = 12), bronchiectasis (n = 8), bronchial wall thickening (n = 4), decreased vascularity (n = 1), and air trapping on expiratory scan (9 of 29 tested). The area affected by these abnormalities, usually involving 2 or more lobes, corresponded in all cases to the location of the infiltrate on chest radiograph at the time of pneumonia. Between subjects with abnormal HRCT (n = 14) and normal HRCT (n = 24) in the pneumonia group, significant differences were observed in age at the time of pneumonia (mean +/- standard deviation: 5.3 +/- 2. 0 years vs 7.7 +/- 3.4 years) and peak antimycoplasma antibody titer (geometric mean [range of 1 standard deviation]; 1:7943 [3126-19 953] vs 1:3093 [832-11 482]). CONCLUSIONS: We conclude that a considerable proportion of children with history of Mycoplasma pneumonia have abnormal findings on HRCT, suggestive of small airway obstruction and that younger age and higher antibody titer at the time of pneumonia may be risk factors for these sequelae.

Antibodies, Bacterial↗
PubMed2000

Genetic and physical mapping of a type 1 diabetes susceptibility gene (IDDM12) to a 100-kb phagemid artificial chromosome clone containing D2S72-CTLA4-D2S105 on chromosome 2q33.

Polymorphic markers within the CTLA4 gene on chromosome 2q33 have been shown to be associated with type 1 diabetes. Therefore, a gene responsible for the disease (IDDM12) most likely lies within a region of <1-2 cM of CTLA4. To define more precisely the IDDM12 interval, we genotyped a multiethnic (U.S. Caucasian, Mexican-American, French, Spanish, Korean, and Chinese) collection of 178 simplex and 350 multiplex families for 10 polymorphic markers within a genomic interval of approximately 300 kb, which contains the candidate genes CTLA4 and CD28. The order of these markers (D2S346, CD28, GGAA19E07, D2S307, D2S72, CTLA4, D2S105, and GATA52A04) was determined by sequence tagged site content mapping of bacterial artificial chromosome (BAC) and yeast artificial chromosome (YAC) clones. The transmission disequilibrium test (TDT) analyses of our data revealed significant association/linkage with three markers within CTLA4 and two immediate flanking markers (D2S72 and D2S105) on each side of CTLA4 but not with more distant markers including the candidate gene CD28. Tsp analyses revealed significant association only with the three polymorphic markers within the CTLA4 gene. The markers linked and associated with type 1 diabetes are contained within a phagemid artificial chromosome clone of 100 kb, suggesting that the IDDM12 locus is either CTLA4 or an unknown gene in very close proximity.

Abatacept↗
PubMed1999

Purification and characterization of heparan sulphate proteoglycan from bovine brain.

A heparan sulphate proteoglycan was purified from adult bovine brain tissues and its structure was characterized. The major heparan sulphate proteoglycan from whole bovine brain had a molecular mass of >200 kDa on denaturing SDS/PAGE and a core protein size of 66 kDa following the removal of glycosaminoglycan chains. Fractionation on DEAE-Sephacel showed that this proteoglycan consisted of three major forms having high, intermediate and low overall charge. All core proteins were identical in size and reacted with heparan sulphate proteoglycan-stub antibody and an antibody made to a synthetic peptide based on rat glypican. The three forms of proteoglycans had identical peptide maps and their amino acid compositional analysis did not match any of the known glypicans. The internal sequence of a major peptide showed only 37.5% sequence similarity with human glypican 5. The glycosaminoglycan chain sizes of the three forms of this proteoglycan, determined after beta-elimination by PAGE, were identical. The disaccharide compositional analysis on the heparan sulphate chains from the three forms of the proteoglycan, determined by treatment with a mixture of heparin lyases followed by high-resolution capillary electrophoresis, showed that they differed primarily by degree of sulphation. The most highly sulphated proteoglycan isolated had a disaccharide composition similar to heparan sulphate glycosaminoglycans found in brain tissue. Based on their sensitivity to low pH nitrous acid treatment, the N-sulphate groups in these proteoglycans were found to be primarily in the smaller glycosaminoglycan chains. The heparan sulphate proteoglycans were also heavily glycosylated with O-linked glycans and no glycosylphosphatidylinositol anchor could be detected.

Amino Acids↗
PubMed1999

Molecular cloning and biological activity of ecdysis-triggering hormones in Drosophila melanogaster.

Ecdysis-triggering hormones (ETH) initiate a defined behavioral sequence leading to shedding of the insect cuticle. We have identified eth, a gene encoding peptides with ETH-like structure and biological activity in Drosophila melanogaster. The open reading frame contains three putative peptides based on canonical endopeptidase cleavage and amidation sites. Two of the predicted peptides (DrmETH1 and DrmETH2) prepared by chemical synthesis induce premature eclosion upon injection into pharate adults. The promoter region of the gene contains a direct repeat ecdysteroid response element. Identification of eth in Drosophila provides opportunities for genetic manipulation of endocrine and behavioral events underlying a stereotypic behavior.

Amino Acid Sequence↗
PubMed1999

Autoradiographic study of NMDA-displaceable [3H]glutamate and [3H]MK-801 binding during butorphanol withdrawal in the rat brain.

Influences of continuous administration of butorphanol on the autoradiography of [3H]glutamate binding and [3H]MK-801 binding were investigated to study the effects of butorphanol withdrawal on NMDA receptors. Rats were administered butorphanol (26 nmol microl(-1) h(-1)) by continuous intracerebroventricular (i.c.v.) infusion through pre-implanted cannula connected to osmotic mini-pumps for 3 days. Rats were then sacrificed at 2, 7, and 24 h after discontinuation of butorphanol infusion. [3H]MK-801 binding was slightly increased in the cortical area, hippocampus, and cerebellum in 2, 7, and 24 h withdrawal groups and was shown most significant increase in the 7 h withdrawal group. NMDA-displaceable [3H]glutamate binding was markedly increased in the cortical area, striatum, septum, hippocampus, thalamus, and cerebellum in 7 h withdrawal group and was significantly increased in the striatum, hippocampus, and thalamus in 24 h withdrawal group. These results demonstrate that the development of butorphanol withdrawal is more prominent by 7 h after discontinuation of butorphanol infusion and suggest that NMDA binding sites at NMDA receptors may play more important role in the development of butorphanol withdrawal than that of channel blocking sites.

Animals↗
PubMed1999

Effect of specific production rate of recombinant protein on multimerization of plasmid vector and gene expression level.

In fed-batch cultures of recombinant Escherichia coli BL21(DE3)[pT7-G3IL2] at high cell concentration, the post-induction specific growth rate was carefully regulated by controlled medium feed to maximize the synthesis level of recombinant fusion interleukin-2, G3.IL-2. A maximum concentration of G3.IL-2 (11.25 g l(-1)) was achieved in the induced recombinant culture growing at the rate of 0.056 h(-1). A steep decrease in the expression level of G3.IL-2 was observed at the post-induction specific growth rates higher than its optimal value (0.056 h(-1)). In the induced recombinant cultures, plasmid multimerization was observed and highly dependent on specific growth and production rate: a higher post-induction specific growth rate and an increased specific production rate tended to significantly promote it much further. Moreover, plasmid stability was found to decrease rapidly in a faster growing culture.

Escherichia coli↗
PubMed1999

Mechanisms that mediate negative regulation of the thyroid-stimulating hormone alpha gene by the thyroid hormone receptor.

A group of transcriptional cofactors for nuclear hormone receptors, referred to as corepressors (CoRs) and coactivators (CoAs), has been shown to induce transcriptional silencing and hormone-induced activation, respectively, of genes that contain positive hormone response elements. Transcriptional silencing by CoRs involves the recruitment of histone deacetylases (HDACs), whereas ligand-dependent activation is associated with the recruitment of CoAs, which possess or recruit histone acetyltransferases (HATs). In a reciprocal manner, negatively regulated genes are stimulated by nuclear receptors in the absence of ligand and are repressed in response to ligand binding to receptors. We show here that negative regulation of the thyroid-stimulating hormone alpha (TSHalpha) promoter by the thyroid hormone receptor (TR) involves a novel mechanism in which the recruitment of CoRs by TR is associated with transcriptional stimulation and histone acetylation. Expression of excess HDAC reverses the stimulation mediated by the TR.CoR complex, consistent with a pivotal role for acetylation in this event. Addition of the ligand, 3,5,3'-triiodothyronine (T3), induces transcriptional repression of the TSHalpha promoter and is associated with the loss of histone acetylation. T3-dependent repression is blocked by phosphorylation of cAMP response element binding protein, or by inhibition of HDAC, indicating that receptor action is subverted by maneuvers that stimulate histone acetylation of the target gene. We propose that negative regulation of a subset of genes by TR involves the active exchange of CoRs and CoAs with intrinsic promoter regulatory elements that normally strongly induce histone acetylation and transcriptional activation.

Acetylation↗
PubMed1999

Molecular interactions in ribose transport: the binding protein module symmetrically associates with the homodimeric membrane transporter.

The Escherichia coli high-affinity ribose transporter is composed of the periplasmic ribose-binding protein (RBP or RbsB), the membrane component (RbsC) and the ATP-binding protein (RbsA). In order to dissect the molecular interactions initiating the transport process, RbsC suppressors for transport-defective rbsB mutations were isolated. These suppressors are localized in two regions of RbsC, which are allele-specific to N- or C-terminal domain mutations of RBP, suggesting that there are two distinct regions of RbsC, each interacting with one of the two domains of RBP. To demonstrate that these two regions provide a homodimeric binding surface for RBP we constructed a dimeric rbsC in which two genes are joined tandemly from head to tail with the addition of a linker. The dimeric RbsC protein is stable and functional in growth and ribose uptake. By exploiting the allele specificity between the domain-specific mutations and their suppressors, we generated all mutation-suppressor combinations in a single rbsB plus the dimeric rbsC genes. Their phenotypes are consistent with the proposal that the binding protein module interacts symmetrically with homodimeric RbsC. The mode of association proposed here for the ribose transport components could be extended to other ABC transporters with similar structural organizations.

ATP-Binding Cassette Transporters↗
PubMed1999

A mutated PtsG, the glucose transporter, allows uptake of D-ribose.

Mutations arose from an Escherichia coli strain defective in the high (Rbs/ribose) and low (Als/allose and Xyl/xylose) affinity D-ribose transporters, which allow cells to grow on D-ribose. Genetic tagging and mapping of the mutations revealed that two loci in the E. coli linkage map are involved in creating a novel ribose transport mechanism. One mutation was found in ptsG, the glucose-specific transporter of phosphoenolpyruvate:carbohydrate phosphotransferase system and the other in mlc, recently reported to be involved in the regulation of ptsG. Five different mutations in ptsG were characterized, whose growth on D-ribose medium was about 80% that of the high affinity system (Rbs+). Two of them were found in the predicted periplasmic loops, whereas three others are in the transmembrane region. Ribose uptakes in the mutants, competitively inhibited by D-glucose, D-xylose, or D-allose, were much lower than that of the high affinity transporter but higher than those of the Als and Xyl systems. Further analyses of the mutants revealed that the rbsK (ribokinase) and rbsD (function unknown) genes are involved in the ribose transport through PtsG, indicating that the phosphorylation of ribose is not mediated by PtsG and that some unknown metabolic function mediated by RbsD is required. It was also found that D-xylose, another sugar not involved in phosphorylation, was efficiently transported through the wild-type or mutant PtsG in mlc-negative background. The efficiencies of xylose and glucose transports are variable in the PtsG mutants, depending on their locations, either in the periplasm or in the membrane. In an extreme case of the transmembrane change (I283T), xylose transport is virtually abolished, indicating that the residue is directly involved in determining sugar specificity. We propose that there are at least two domains for substrate specificity in PtsG with slightly altered recognition properties.

Binding Sites↗
PubMed1999

Oregon's low in-hospital death rates: what determines where people die and satisfaction with decisions on place of death?

Where Americans die is much more influenced by what part of the country they live in than by what their preferences are for location of death. Although most Americans report a preference for death at home, a majority still die in acute care hospitals. We describe the experiences of patients who died in Oregon (the state that currently has the lowest in-hospital death rate in the United States--31%) and the views of their families. We examine the factors influencing respect for dying patients' preferred location of death. Data from Oregon studies confirm that decisions to avoid hospital admission are far more common than discharge of the actively dying. Do-not-resuscitate orders were reported for 91% of nursing home residents in one study and living wills were reported for 67% of a random sample of adult Oregon decedents in a second study. In the second study, decisions not to start treatment were far more common than decisions to stop treatment (79% compared with 21%). Only 2.4% of families reported that "too little" treatment was given. Throughout the United States, use and availability of beds in acute care hospitals have been confirmed to be the principal determining factors in location of death. Within that constraint, however, the availability of other resources and services both facilitates the process of arranging for patients to die outside the hospital and improves satisfaction with the quality of terminal care.

Advance Care Planning↗
PubMed1999

Heparin binding and augmentation of C1 inhibitor activity.

Heparin and other glycosaminoglycans have profound activity in vitro on the regulation of complement activity. The studies reported here examined the mechanism whereby heparin enhances C1 esterase inhibitor (C1INH) activity on C1 esterase (C1). The interaction of heparin and heparan sulfate with C1INH was first examined using surface plasmon resonance. Heparin was immobilized on a biosensor chip in two orientations, at its reducing end and in midchain, and heparan sulfate was immobilized at its reducing end. Heparin immobilized at its reducing end interacted with C1INH, giving an association constant (Ka) value of 1.43 x 10(7) M-1, whereas heparin immobilized in midchain afforded a Ka value of 7 x 10(6) M-1. No interaction between C1INH and heparan sulfate could be observed. Next, the augmentation of C1INH by heparin (Mr (av) 13,000), low-molecular-weight (LMW) heparin (Mr (av) 5000), and heparan sulfate (Mr (av) 11,000) was determined. C1INH alone was at least 10, 000 times more active in inhibiting fluid phase C1 compared with erythrocyte-bound C1 (EAC1). When C1 was in the fluid phase, both heparin and LMW heparin were relatively ineffective at augmenting C1INH activity on C1. In contrast, when C1 was present as EAC1, heparin augmented C1INH activity at all C1INH concentrations examined and LMW heparin was up to 1.3 times more effective than heparin. This augmentation only occurred when both C1INH and heparin were present together with the EAC1. Hence, although surface plasmon resonance shows that heparin binds to C1INH, heparin augmentation of C1INH activity appears to require a terniary complex in which cell bound C1 interacts with both heparin and C1INH. This is the first report of LMW heparin augmenting C1INH activity. Heparan sulfate neither interacted with C1INH nor did it augment C1INH activity.

Adjuvants, Pharmaceutic↗
PubMed1999

Lamivudine for chronic delta hepatitis.

Chronic delta hepatitis is a severe form of chronic liver disease caused by hepatitis delta virus (HDV) infection superimposed on chronic hepatitis B or the hepatitis B surface antigen (HBsAg) carrier state. Therapy of delta hepatitis is currently unsatisfactory. We have evaluated lamivudine (3-thiacytidine), an oral nucleoside analogue with marked effects against hepatitis B, as therapy in 5 patients with chronic hepatitis D. Five men, ages 38 to 65 years, were treated. All had HBsAg, antibody to HDV, and HDV RNA in serum, as well as persistent elevations in alanine aminotransferase (ALT) levels and liver histology showing severe chronic hepatitis with fibrosis or cirrhosis. Lamivudine was given in a dose of 100 mg orally daily for 12 months. Patients were monitored carefully and tested for HBsAg, HBV-DNA and HDV-RNA levels serially during the year of treatment and for 6 months thereafter. Liver biopsies were performed before therapy and repeated after 1 year. Serum levels of HBV DNA fell rapidly in all 5 patients, becoming undetectable even by polymerase chain reaction (PCR) in 4. However, all 5 patients remained HBsAg- and HDV-RNA-positive, and serum ALT levels and liver histology did not improve. All patients tolerated therapy well. When lamivudine was stopped, HBV-DNA levels returned to pretreatment values without a change in disease activity. Lamivudine is a potent inhibitor of HBV-DNA replication, but does not improve disease activity or lower HDV-RNA levels in patients with chronic delta hepatitis.

Adult↗
PubMed1999

Neurilemmoma of the mandible.

Intraosseous neurilemmoma is rare, representing less than 1% of benign primary bone tumors. The site most commonly involved is the mandible. We report on a neurilemmoma of the mandible in a 30-year-old woman. A panoramic radiograph of the mandible showed a well-defined unilocular osteolytic lesion with a thin uniform sclerotic margin located in the body of the mandible. The CT scan confirmed a well-defined osteolytic lesion with thinning of the cortex of the body of the left side of the mandible. Histologically, the lesion was a moderately cellular neoplasm with distinct palisading and numerous Verocay bodies. Ultrastructurally, the cytoplasmic membranes were distinct and coated by amorphous bands of basal lamina. Complete excision was achieved by removing the tumor from the inferior alveolar nerve.

Adult↗