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Biomedical subjects

Stacie M Jones

Publications and source records attributed to Stacie M Jones.

16 recordsLinked to original sources
PubMed2006

Egg oral immunotherapy in nonanaphylactic children with egg allergy.

BACKGROUND: There is no current active treatment for food allergy. Traditional injection immunotherapy has been proved unsafe, and thus there is a need for other forms of immunotherapy. OBJECTIVE: The purpose was to study the safety and immunologic effects of egg oral immunotherapy (OIT). The short-term goal was to desensitize subjects to protect against accidental ingestion reactions. The eventual goal was to induce lasting clinical and immunologic tolerance. METHODS: Subjects with a history of egg allergy but without a history of anaphylaxis to egg underwent a 24-month egg OIT protocol involving modified rush, build-up, and maintenance phases. Double-blind, placebo-controlled food challenges were performed at study conclusion. Egg-specific IgE and IgG concentrations were followed. RESULTS: Seven subjects completed the protocol. Egg-specific IgG concentrations increased significantly, whereas egg-specific IgE concentrations did not significantly change. Three subjects tolerated known or possible accidental egg ingestions while receiving OIT. During double-blind, placebo-controlled food challenges at study conclusion, all tolerated significantly more egg protein than at study onset and than that found in the typical accidental exposure. Two subjects demonstrated oral tolerance. CONCLUSION: This study provides proof of concept that OIT can be safely used for patients with egg allergy without a history of anaphylaxis to egg. Egg OIT does not heighten sensitivity to egg and might protect against reaction on accidental ingestion. Whether OIT will induce clinical oral tolerance cannot be concluded from this initial cohort. CLINICAL IMPLICATIONS: Use of allergen-specific OIT to protect subjects with food allergy from reaction on accidental ingestion would represent a significant paradigm change in the treatment of food allergy.

Administration, Oral↗
PubMed2006

Allergic fungal sinusitis in children.

BACKGROUND: Allergic fungal sinusitis (AFS) has been characterized in adults presenting with chronic sinusitis. Rare reports allude to a similar disease in children. OBJECTIVE: To characterize the features of AFS in children. METHODS: Children referred to otolaryngology clinics at Arkansas and LeBonheur Children's Hospitals for chronic sinusitis during a 12-year period were studied. This retrospective analysis reviews the following: clinical presentation, laboratory evaluations, radiographic and pathologic findings, and surgical intervention. Twenty patients (age range, 7-18 years; mean age, 12.5 years; median age, 16 years) met previously published criteria for AFS. Thirteen patients were male and 7 were female. Thirteen were African American and 7 were white. RESULTS: Presentation at diagnosis included the following: atopy (n = 20), nasal symptoms (n = 20), recurrent sinusitis (n = 18), nasal polyps (n = 18), recurrent headaches (n = 12), asthma (n = 11), proptosis (n = 10), and ocular symptoms (n = 10). All had radiographic evidence of sinusitis and allergy to fungal organisms. IgE levels were elevated in 8 of 9 patients, and 10 of 15 patients had eosinophilia. Surgical specimens demonstrated allergic mucin (n = 11), Charcot-Leyden crystals (n = 2), hyphae or fungal debris (n = 9), and fungal growth (n = 17). All patients underwent endoscopic sinus surgery, with 11 requiring multiple surgical procedures. Postoperatively, 19 patients received intranasal and oral steroids, and all had nasal saline washes. Eleven patients (9 who had undergone multiple surgical procedures) were treated with immunotherapy. Relapse was seen in 55% of patients at 1 year of follow-up. CONCLUSION: AFS presents with a higher incidence of proptosis in children when compared with adults. Typically, AFS occurs in atopic children with refractory sinus disease, requiring a high index of suspicion for evaluation and aggressive treatment.

Adolescent↗
PubMed2006

Symptom profile and asthma control in school-aged children.

BACKGROUND: Children with poorly controlled asthma are at high risk of airway remodeling, sleep disruption, school absenteeism, and limited participation in activities. OBJECTIVE: To determine asthma prevalence and characterize disease severity and burden in school-aged children. METHOD: A case-finding study was conducted via a multiple-choice questionnaire and asthma algorithm. Items used for analysis include physician diagnosis of asthma, symptom severity, and health care utilization. The chi2 test was used to determine the significance of differences among cases. Logistic regression was used to evaluate the association of patient factors and asthma indicators. RESULTS: Of the 5,417 children surveyed, 1,341 (25%) were classified as being at risk of asthma. Of these asthma cases, 55% were positive by diagnosis and algorithm (active), 10% were positive per algorithm alone (suspected), and 35% were positive per diagnosis alone (nonactive). Only 14% of all asthma cases reported experiencing no respiratory symptoms (< 1% active, 2% suspected, and 40% nonactive) compared with 75% of noncases. Also, 75% of noncases reported never missing school compared with 19%, 33%, and 54% of active, suspected, and nonactive asthma cases. African American race, Medicaid enrollment, and male sex were independent predictors of asthma risk. Similarly, African American race, Medicaid enrollment, age, and persistent asthma were independent predictors of emergency department use among asthma cases. DISCUSSION: Prevalence of active symptoms suggestive of poor asthma control was extremely high among urban, minority children enrolled in Arkansas' largest public school district. Poor asthma control greatly affects quality of life, including school attendance and performance. Interventions should raise expectations and emphasize the importance of achieving asthma control.

Adolescent↗
PubMed2006

X-linked agammaglobulinemia: report on a United States registry of 201 patients.

X-linked agammaglobulinemia (XLA) is a primary immunodeficiency caused by mutations in the gene for Bruton tyrosine kinase (BTK) that result in the deficient development of B lymphocytes and hypogammaglobulinemia. Because the disorder is uncommon, no single institution has had sufficient numbers of patients to develop a comprehensive clinical picture of the disorder. Accordingly, a national registry of United States residents with XLA was established in 1999 to provide an updated clinical view of the disorder in a large cohort of patients. A total of 201 patients were registered by 66 physicians. The estimated birth rate for the 10-year period of 1988-1997 was 1/379,000. Infection was the most common initial clinical presentation (85%), followed by a positive family history (41%) and neutropenia (11%). Although the average age of diagnosis was younger in patients with a positive family history (mean, 2.59 yr) than in patients with a negative family history (mean, 5.37 yr) (p < 0.001), only 34.5% of patients with a positive family history at the time of their birth were diagnosed before clinical symptoms developed-that is, based on family history alone. Seventy percent of patients had at least 1 episode of otitis, 62% at least 1 episode of pneumonia, 60% at least 1 episode of sinusitis, 23% at least 1 episode of chronic/recurrent diarrhea, 21% at least 1 episode of conjunctivitis, 18% at least 1 episode of pyoderma and/or cellulitis, 11% at least 1 episode of meningitis/encephalitis, 10% at least 1 episode of sepsis, 8% at least 1 episode of septic arthritis, 6% at least 1 episode of hepatitis, and 3% at least 1 episode of osteomyelitis. Fourteen of 201 (6.9%) patients were dead at the time they were entered in the Registry. However, in a prospective 4 /4-year follow-up of living patients, only 3/80 (3.75%) patients died. Causes of death included disseminated enterovirus infection (n = 6), pulmonary insufficiency (n = 5), adenovirus infection (n = 1), sepsis (n = 1), acquired immunodeficiency disease syndrome (AIDS) (n = 1), myocarditis (n = 1), hepatitis (n = 2), and stem cell transplantation (n = 1).

Adolescent↗
PubMed2006

School-based asthma case finding: the Arkansas experience.

This population-based case-finding study sought to determine asthma prevalence and characterize disease severity and burden among school-aged children in the Little Rock School District. Asthma cases were identified by validated algorithm and parental report of asthma diagnosis. The overall response rate was low. Among schools with greater than 50% response rate, prevalence of physician-diagnosed asthma was comparable to other studies in public school settings. Prevalence of symptoms in cases identified as current is suggestive of poor asthma control. Improved systems for case identification of children with asthma are needed in schools. Efforts should focus on strategies to improve asthma control.

Adolescent↗
PubMed2006

Spine bone densitometry in asthmatic children treated with high dose corticosteroids: correcting for racial discrepancies.

PURPOSE: Our hypothesis is that the use of standards based on Caucasian children will under-estimate the incidence of abnormal bone density in African American children. MATERIALS AND METHODS: Eighty-two African American and 80 Caucasian asthmatic children classified as high-dose inhaled corticosteroid users comprised the study population. Bone mineral density measurements were compared to reference standards, based on Caucasians, to calculate Z-values. Regression analysis was used to compare Z-values derived from the race-specific and Caucasian standards for 32 African American children. The derived regression analysis equation was then applied to the entire African American population to determine the incidence of abnormal bone density. RESULTS: The asthmatic Caucasian mean spine bone density was significantly less than the normal standards (p < .001), but the African American mean spine bone density was not, despite the high-dose steroid use. Using the Caucasian standards, Caucasians were significantly more likely to have abnormal bone density detected (p < 0.015). Regression analysis of the 32 children with available race specific standards resulted in the following equation: Z African American= Z Caucasian-0.86. The number of African Americans with abnormal bone density detected using the regression equation was not significantly different than the Caucasian children (p > 0.12). CONCLUSIONS: Asthmatic African Americans treated with high-dose inhaled corticosteroids had denser bones than Caucasians. Caucasian standards can be adjusted using a regression equation.

Absorptiometry, Photon↗
PubMed2005

The beta-agonist isoproterenol attenuates EGF-stimulated wound closure in human airway epithelial cells.

Asthma is a disease characterized by reversible airway obstruction. An additional hallmark of chronic asthma is altered wound healing that leads to airway remodeling. Although beta-agonists are effective in treating the bronchospasm associated with asthma, their effects on airway wound healing, which are related to airway remodeling, are unknown. It has been demonstrated that beta-agonists can alter the signaling of epidermal growth factor (EGF) receptors, which are important in timely wound healing. Therefore, we hypothesized that the beta-agonist isoproterenol would affect wound healing. Using an in vitro scrape wound assay, we demonstrated that isoproterenol attenuates EGF-stimulated wound healing in 16HBE airway epithelial cell cultures. Through experiments with forskolin and cells overexpressing beta2-adrenergic receptor-yellow fluorescent protein, we show that attenuation is due to the accumulation of cAMP and the involvement of at least one additional pathway. Furthermore, attenuation is not due to a direct effect on the EGF receptor or to an alteration of the ERK/MAPK signaling cascade. Based on these results, we propose that isoproterenol may exert its effects through other MAPK signaling pathways (JNK and/or p38) or through parallel mechanisms. These results also demonstrate a problem of potential therapeutic relevance in which a commonly prescribed medication may alter wound healing and contribute to the remodeling of asthmatic airways.

Adrenergic beta-Agonists↗
PubMed2004

Coordinating epidermal growth factor-induced motility promotes efficient wound closure.

Wound healing is a response to injury that is initiated to reconstruct damaged tissue. In skin, reepithelialization involves both epithelial cells and fibroblasts and contributes to the reformation of a barrier between the external environment and internal milieu. Growth factors including epidermal growth factor (EGF) play important roles in promoting this process. In the present studies we employed CV-1 fibroblasts in a tissue culture model of reepithelialization to develop strategies for optimizing wound closure stimulated by EGF. We found that EGF enhanced cell motility within 6-8 h of EGF treatment in serum-free medium but wounds failed to close within 24 h. However, if medium on these cultures was exchanged for medium containing serum, cells pretreated with EGF closed new scrape wounds more rapidly than did cells that were not pretreated. These results indicate that serum factors work in concert with EGF to coordinate cell motility for efficient wound closure. Indeed, EGF enhanced the rate of wound closure in the presence of serum, and this effect also persisted for at least 24 h after EGF was removed. This coordination of EGF-induced cell motility was accompanied by an increase in the transient phosphorylation of ERK1 and ERK2. The persistent effects of EGF were blocked by transient exposure to reversible inhibitors of transcription and translation, indicating that the expression of new proteins mediated this response. We propose that EGF-stimulated CV-1 fibroblast motility is coordinated by a serum component that induces cell-cell adhesive properties consistent with an epithelial phenotype, thereby enhancing the reepithelialization process.

Animals↗
PubMed2004

Characteristics of children with asthma who are enrolled in a Head Start program.

BACKGROUND: Asthma is an increasing public health concern that disproportionally affects children. In 1998, the Centers for Disease Control identified children aged 0 to 4 years as the "driving force" behind climbing rates of asthma-related emergency department visits and hospitalizations. Despite the significant asthma burden in preschool children, few studies characterize this population. OBJECTIVE: This study identifies and characterizes children at risk for asthma who are enrolled in a local Head Start program. METHODS: Caregivers of 368 children aged 3 to 5 years who were identified by using an asthma survey were recruited. Data were collected on demographics, health care use and access, medication use, symptoms, and trigger exposure. Exposure to tobacco smoke was determined by urinary cotinine and allergen sensitization by skin prick test. RESULTS: At baseline, 64% of the children had more than 1 emergency department visit for asthma in their lifetime, whereas 31% had more than 1 visit in the previous 6 months. Caretakers reported smoking in 37% of households with cotinine exceeding 20 ng/mg in 27% of the sample. Twenty-one percent reported symptoms consistent with intermittent asthma, and 79% reported symptoms consistent with persistent asthma. Forty-five percent of the children reported nighttime symptoms more than 1 night per week. Seventy-one percent had positive test results for more than 1 allergen, and 42% had positive test results for more than 3 allergens. Only 32% of children with persistent asthma had both rescue and controller medications. CONCLUSION: Children with asthma enrolled in a Head Start program have significant environmental tobacco smoke exposure, are highly atopic and symptomatic, and do not receive appropriate medication treatment. Overall, children in the study had poor asthma control. This high-risk group could benefit from case management programs.

Black or African American↗
PubMed2003

Enhanced beta2-adrenergic receptor (beta2AR) signaling by adeno-associated viral (AAV)-mediated gene transfer.

BACKGROUND: Beta2-adrenergic receptors (beta2AR) play important regulatory roles in a variety of cells and organ systems and are important therapeutic targets in the treatment of airway and cardiovascular disease. Prolonged use of beta-agonists results in tolerance secondary to receptor down-regulation resulting in reduced therapeutic efficiency. The purpose of this work is to evaluate the signaling capabilities of the beta2AR expressed by a recombinant adeno-associated viral (AAV) vector that also included an enhanced green fluorescent protein (EGFP) gene (AAV-beta2AR/EGFP). RESULTS: By epifluorescence microscopy, approximately 40% of infected HEK 293 cells demonstrated EGFP expression. beta2AR density measured with [3H]dihydroalprenolol ([3H]DHA) increased either 13- or 77-fold in infected cells compared to mock infected controls depending on the culture conditions used. The [3H]DHA binding was to a single receptor population with a dissociation constant of 0.42 nM, as would be expected for wild-type beta2AR. Agonist competition assays with [3H]DHA showed the following rank order of potency: isoproterenol>epinephrine> norepinephrine, consistent with beta2AR interaction. Isoproterenol-stimulated cyclic AMP levels were 5-fold higher in infected cells compared to controls (314 +/- 43 vs. 63.4 +/- 9.6 nmol/dish; n = 3). Receptor trafficking demonstrated surface expression of beta2AR with vehicle treatment and internalization following isoproterenol treatment. CONCLUSIONS: We conclude that HEK 293 cells infected with AAV-beta2AR/EGFP effectively express beta2AR and that increased expression of these receptors results in enhanced beta2AR signaling. This method of gene transfer may provide an important means to enhance function in in vivo systems.

Adenoviridae↗
PubMed2003

Molecular cloning and functional characterization of a vasotocin receptor subtype expressed in the pituitary gland of the domestic chicken (Gallus domesticus): avian homolog of the mammalian V1b-vasopressin receptor.

The neurohypophysial hormone arginine vasotocin (AVT) stimulates adrenocorticotropin hormone (ACTH) secretion from the avian anterior pituitary gland resulting in increased adrenal secretion of corticosterone in response to stress. Here, we report molecular cloning and functional characterization of a gene encoding an AVT receptor subtype, designated the VT2 receptor, that may mediate the stimulatory effect of AVT on ACTH secretion in birds. The open reading frame predicts a 425 amino acid polypeptide that includes seven segments of 19 to 24 hydrophobic amino acids, typical of guanine nucleotide-protein coupled receptors. Phylogenetic analysis revealed that the VT2 receptor shares highest identity with the mammalian V1b-vasopressin receptor subtype. Expressed VT2 receptors in COS7 cells mediate AVT-induced phosphatidylinositol turnover and Ca(2+) mobilization. In the domestic chicken, expression of VT2 receptor gene transcripts is limited to the pituitary gland. Based on similarities in sequence, site of expression and coupled signal transduction pathways, we conclude that the VT2 receptor is the avian homolog of the mammalian V1b-vasopressin receptor, and therefore may play an important role in the avian stress response.

Amino Acid Sequence↗
PubMed2003

Occupational asthma symptoms and respiratory function among aerial pesticide applicators.

BACKGROUND: Pesticide exposure has been suggested as one causal factor for the rise in asthma prevalence. The goal of this investigation was to determine the effect of pesticide exposure on respiratory symptoms and lung function in workers with occupational exposure to pesticides. METHODS: A prospective, case-controlled study was conducted among pesticide aviators (AV) and community controls (Con). In Phase I, subjects completed an asthma survey and baseline spirometry. In Phase II, subjects reported symptoms, lung function monitoring, and pesticide exposure during two, 14-day periods. RESULTS: Phase I-Self-reported asthma and symptoms were similar among AV (n = 135) and Con (n = 118) with 4-6% prevalence reported but with higher rates among smokers. Baseline lung function was similar; although, a higher proportion of AV had forced expiratory volume in one second (FEV(1)) <80% predicted (8% vs. 2%, P = 0.02). Phase II-Self-reported symptoms were similar with 80% of AV (n = 50) and 73% of Con (n = 49) reporting no symptoms. Only 4% of AV and 6% of controls reported increased symptoms from baseline to spray season. Serial lung function did not differ between group and mean diurnal variation in peak expiratory flow improved in both groups between sampling times (AV 18% vs. 14%; Con 19% vs. 16%, P < 0.001). CONCLUSIONS: This study suggests that among workers with occupational pesticide exposure, asthma symptoms and lung function are similar to those of controls with only community-based exposure.

Adult↗
PubMed2002

Access to spacers and peak flow meters among medicaid patients with asthma.

Asthma morbidity and mortality have increased at alarming rates. Morbidity is significantly higher among minorities and low-income populations. The purpose of this study was to survey pharmacies licensed to provide both asthma medications and durable medical equipment (DME) to evaluate their acceptance of Medicaid as payment for spacers and peak flow meters in patients with Medicaid. Twenty-four pharmacies were identified and completed a telephone survey. Only 64% of the pharmacies licensed to accept Medicaid for DME provide this service. We postulate that improving DME licensing and claims reimbursement will impact medication compliance, as well as asthma morbidity and mortality.

Anti-Asthmatic Agents↗
PubMed2002

EGF receptor downregulation depends on a trafficking motif in the distal tyrosine kinase domain.

On binding to its receptor, epidermal growth factor (EGF) initiates a cascade of events leading to cell proliferation or differentiation. In addition, the EGF receptor itself is downregulated to attenuate mitogenic signaling. Downregulation occurs through trafficking of receptors to lysosomes, culminating in proteolytic destruction of both the receptor and ligand; however, endocytic sorting mechanisms that underlie lysosomal targeting remain obscure. The goal of this study was to explore one aspect of the molecular basis for ligand-induced lysosomal targeting and degradation of EGF receptors. In this study, we identify a tyrosine-leucine motif ((954)YLVI) that is essential for transit of ligand-receptor complexes to lysosomes. When this motif is mutated, HEK 293 cells expressing the mutant receptors demonstrate impaired lysosomal targeting and downregulation compared with wild-type receptors. (954)YLVI is highly conserved among EGF receptors from various mammalian and invertebrate species and is critical for receptor downregulation. We propose that (954)YLVI works in concert with at least two additional regions within the EGF receptor cytoplasmic domain that are essential for efficiently targeting ligand-receptor complexes to the lysosome.

Amino Acid Motifs↗