Biomedical subjects

Jie Huang

Publications and source records attributed to Jie Huang.

At least 55 records · Page 3Linked to original sources

PubMed2005

Enhancement of cisplatin sensitivity of cisplatin-resistant human cervical carcinoma cells by bryostatin 1.

PURPOSE: Bryostatin 1, a unique protein kinase C (PKC) activator, is already in the clinical trials. An understanding of complex regulation of PKC by bryostatin 1 is essential for effective use of bryostatin 1 in the clinic. We have previously shown that the ability of bryostatin 1 to enhance cisplatin sensitivity correlated with its ability to down-regulate PKCdelta in HeLa cells. We have investigated how bryostatin 1 influences PKCdelta regulation in cisplatin-resistant HeLa (HeLa/CP) cells, and if bryostatin 1 could be used to reverse cisplatin resistance. EXPERIMENTAL DESIGN: Phorbol 12,13-dibutyrate (PDBu), bryostatin 1, and small interfering RNA were used to manipulate PKC level/activation status. Cell death was monitored by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, Annexin V dye-binding assay, and analysis of hypodiploid peak in a flow cytometer. RESULTS: Bryostatin 1 elicited a biphasic concentration response on PKCdelta down-regulation and cisplatin-induced cell death in HeLa/CP cells; the maximum effect was achieved with 1 nmol/L bryostatin 1. Down-regulation of PKCalpha increased with increasing concentrations of bryostatin 1. PDBu induced down-regulation of PKCalpha in HeLa and HeLa/CP cells but it had little effect on PKCdelta down-regulation in HeLa/CP cells. However, both PDBu and bryostatin 1 enhanced the sensitivity of HeLa/CP cells to cisplatin. Knockdown of PKCdelta by small interfering RNA inhibited cisplatin-induced apoptosis but knockdown of PKCalpha enhanced cisplatin-induced cell death. CONCLUSIONS: These results suggest that although PKCdelta acts as a proapoptotic protein, full-length PKCdelta may inhibit cisplatin-induced cell death. Thus, persistent activation/down-regulation of PKCdelta by bryostatin 1 was associated with cisplatin sensitization. Furthermore, PKCalpha acts as an antiapoptotic protein and down-regulation of PKCalpha by PDBu was associated with cellular sensitization to cisplatin.

Antineoplastic Agents↗

PubMed2005

Four viral proteins of white spot syndrome virus (WSSV) that attach to shrimp cell membranes.

White spot syndrome virus (WSSV) is a major shrimp pathogen that has a widespread negative affect on shrimp production in Asia and the Americas. It is known that WSSV infects shrimp cells through viral attachment proteins (VAP) that bind with shrimp cell receptors. However, the identity of both WSSV VAP and shrimp cell receptors remains unclear. We used digoxigenin (DIG)-labeled shrimp hemocyte and gill cell membranes to bind to WSSV proteins immobilized on nitrocellulose membranes, and 4 putative WSSV VAP (37 kDa, 39 kDa and 2 above 97 kDa) were identified. Mass spectrometric analysis identified the 37 kDa putative VAP as the product of WSSV gene VP281.

Amino Acid Sequence↗

PubMed2005

Ku80 autoantigen as a cellular coreceptor for human parvovirus B19 infection.

Human parvovirus B19 (B19) infects human erythroid cells expressing P antigen. However, some cell lines that were positive for P antigen failed to bind B19, whereas some cell lines had an ability to bind B19 despite undetectable expression of P antigen. We here demonstrate that B19 specifically binds with Ku80 autoantigen on the cell surface. Furthermore, transfection of HeLa cells with the gene of Ku80 enabled the binding of B19 and allowed its entry into cells. Moreover, reduction of cell-surface expression of Ku80 in KU812Ep6 cells, which was a high-sensitive cell line for B19 infection, by short interfering RNA for Ku80 resulted in the marked inhibition of B19 binding in KU812Ep6 cells. Although Ku80 originally has been described as a nuclear protein, human bone marrow erythroid cells with glycophorin A or CD36, B cells with CD20, or T cells with CD3 were all positive for cell-surface expression of Ku80. B19 infection of KU812Ep6 cells and bone marrow cells was inhibited in the presence of anti-Ku80 antibody. Our data suggest that Ku80 functions as a novel coreceptor for B19 infection, and this finding may provide an explanation for the pathologic immunity associated with B19 infection.

Antibodies↗

PubMed2005

Surgical treatment of giant esophageal leiomyoma.

AIM: To summarize the operative experiences for giant leiomyoma of esophagus. METHODS: Eight cases of giant esophageal leiomyoma (GEL) whose tumors were bigger than 10 cm were treated surgically in our department from June 1980 to March 2004. All of these cases received barium swallow roentgenography and esophagoscopy. Leiomyoma located in upper thirds of the esophagus in one case, middle thirds of the esophagus in five cases, lower thirds of the esophagus in two cases. Resection of tumors was performed successfully in all of these cases. Operative methods included transthoracic extramucosal enucleation and buttressing the muscular defect with pedicled great omental flap (one case), esophagectomy and esophago-gastrostomy above the arch of aorta (three cases), total esophagectomy and esophageal replacement with colon (four cases). Histological examination confirmed that all of these cases were leiomyoma. RESULTS: All of the eight patients recovered approvingly with no mortality and resumed normal diet after operation. Vomiting during meals occurred in one patient with esophagogastrostomy, and remained 1 mo. Reflux esophagitis occurred in one patient with esophago-gastrostomy and was alleviated with medication. Thoracic colon syndrome (TCS) occurred in one patient with colon replacement at 15 mo postoperatively. No recurrence occurred in follow-up from 6 mo to 8 years. CONCLUSION: Surgical treatment for GEL is both safe and effective. The choices of operative methods mainly depend on the location and range of lesions. We prefer to treat GEL via esophagectomy combined with esophago-gastrostomy or esophagus replacement with colon. The long-time quality of life is better in the latter.

Adult↗

PubMed2005

[Surgery for upper or middle thoracic esophageal carcinoma after gastrectomy].

OBJECTIVE: To evaluate the surgical treatment and technical key-points of upper or middle thoracic esophageal carcinoma in patients with history of gastrectomy. METHODS: Eighty-six patients with upper or middle thoracic esophageal carcinoma after previous gastrectomy received surgical treatment between 1980 and 2004. Among them, tumor location was in middle thoracic esophagus in 50 patients, in upper thoracic esophagus in 31 and cervical esophagus in 5. Postoperative pathological staging was stage I in 16 patients, stage IIa in 62, stage IIb in 5 and stage III in 8. The interval between gastrectomy and the diagnosis of esophageal carcinoma ranged from 2 to 22 years. Surgical procedures included esophagectomy and reconstruction with nonreversed gastric tube in 2 patients and reversed gastric tube in 3. The esophagus was reconstructed with short segment of colon in 5 patients and long segment of colon in 74. Two cases underwent jejunostomy only. RESULTS: Seventy-six patients (88%) were treated with curative intent. Seven patients (8%) received palliative surgery. Postoperative complication rate was 12% (10/86). One patient died of multiple organ dysfunction syndrome (MODS). Sixty-seven patients were followed up, the 1-, 3-, 5-year survival rates were 84% (56/67), 57% (38/67) and 22% (15/67), respectively. CONCLUSIONS: Surgical treatment is the first choice for esophageal cancer patients after gastrectomy although the procedures are complicated. The surgery should be considered as a reliable therapeutic modality because of favorable patient prognosis. The replacement with colon is recommended for those patients.

Adult↗

PubMed2005

Oncogenic Ras increases sensitivity of colon cancer cells to 5-FU-induced apoptosis.

Despite the fact that objective response rates to 5-FU are as low as 20%, 5-FU remains the most commonly used drug for the treatment of colorectal cancer. The lack of understanding of resistance to 5-FU, therefore, remains a significant impediment in maximizing its efficacy. We used intestinal epithelial cells with an inducible K-RasV12 to demonstrate that expression of oncogenic Ras promotes cell death upon 5-FU treatment. Accordingly, transient expression of the mutant RasV12, but not the WT Ras, enhanced 5-FU-induced apoptosis in 293T cells. Consistent with these data, we showed that targeted deletion of the mutant Ras allele in the HCT116 colon cancer cell line protected cells from 5-FU-induced apoptosis. Using isogenic colon cancer cell lines that differ only by the presence of the mutant Ras allele, HCT116 and Hke-3 cells, we demonstrated that signaling by oncogenic Ras promotes both accumulation of p53 and its phosphorylation on serine15 in response to 5-FU, a situation that favors apoptosis over growth arrest. However, despite the differential induction of p53 in HCT116 and Hke-3 cells, the expression of Puma, a gene with an important role in p53-dependent apoptosis, was not affected by Ras signaling. In contrast, we showed that Ras interferes with 5-FU-induced expression of gelsolin, a protein with known antiapoptotic activity. We ascertained the role of gelsolin in 5-FU-induced apoptosis by demonstrating that silencing of gelsolin expression through RNAi sensitized cells to 5-FU-induced apoptosis and that re-expression of gelsolin in cells harboring mutant Ras protected cells from 5-FU-induced apoptosis. These data therefore demonstrate that Ras mutations increase sensitivity to 5-FU-induced apoptosis at least in part through the negative regulation of gelsolin expression. Our data indicate that Ras mutations promote apoptosis in response to 5-FU treatment and imply that tumors with Ras mutations and/or reduced expression of gelsolin may show enhanced apoptosis in response to 5-FU also in vivo.

Apoptosis↗

PubMed2005

Health information technology and physician-patient interactions: impact of computers on communication during outpatient primary care visits.

OBJECTIVE: The aim of this study was to evaluate the impact of introducing health information technology (HIT) on physician-patient interactions during outpatient visits. DESIGN: This was a longitudinal pre-post study: two months before and one and seven months after introduction of examination room computers. Patient questionnaires (n = 313) after primary care visits with physicians (n = 8) within an integrated delivery system. There were three patient satisfaction domains: (1) satisfaction with visit components, (2) comprehension of the visit, and (3) perceptions of the physician's use of the computer. RESULTS: Patients reported that physicians used computers in 82.3% of visits. Compared with baseline, overall patient satisfaction with visits increased seven months after the introduction of computers (odds ratio [OR] = 1.50; 95% confidence interval [CI]: 1.01-2.22), as did satisfaction with physicians' familiarity with patients (OR = 1.60, 95% CI: 1.01-2.52), communication about medical issues (OR = 1.61; 95% CI: 1.05-2.47), and comprehension of decisions made during the visit (OR = 1.63; 95% CI: 1.06-2.50). In contrast, there were no significant changes in patient satisfaction with comprehension of self-care responsibilities, communication about psychosocial issues, or available visit time. Seven months post-introduction, patients were more likely to report that the computer helped the visit run in a more timely manner (OR = 1.76; 95% CI: 1.28-2.42) compared with the first month after introduction. There were no other significant changes in patient perceptions of the computer use over time. CONCLUSION: The examination room computers appeared to have positive effects on physician-patient interactions related to medical communication without significant negative effects on other areas such as time available for patient concerns. Further study is needed to better understand HIT use during outpatient visits.

Adult↗

PubMed2005

Crystal imperfection studies of pure and silicon substituted hydroxyapatite using Raman and XRD.

Hydroxyapatite (HA) is important in biomedical applications because of its chemical similarity to the mineral content of bone and its consequent bioactivity. Silicon substitution into the hydroxyapatite crystal lattice was found to enhance its bioactivity both in vitro and in vivo [1, 2]. However, the mechanism for the enhancement is still not well understood. In this paper, the crystal imperfections introduced by silicon substitution were studied using XRD and Raman spectroscopy. It was found that silicon substitution did not introduce microstrain, but deceased the crystal size in the hk0 direction. Three new vibration modes and peak broadening were observed in Raman spectra following silicon incorporation. The imperfections introduced by silicon substitution may play a role in enhancing bioactivity. A phenomenological relationship between the width of the PO4 v1 peak and crystal size was established.

Crystallization↗

PubMed2005

Neural network-based adaptive dynamic surface control for a class of uncertain nonlinear systems in strict-feedback form.

The dynamic surface control (DSC) technique was developed recently by Swaroop et al. This technique simplified the backstepping design for the control of nonlinear systems in strict-feedback form by overcoming the problem of "explosion of complexity." It was later extended to adaptive backstepping design for nonlinear systems with linearly parameterized uncertainty. In this paper, by incorporating this design technique into a neural network based adaptive control design framework, we have developed a backstepping based control design for a class of nonlinear systems in strict-feedback form with arbitrary uncertainty. Our development is able to eliminate the problem of "explosion of complexity" inherent in the existing method. In addition, a stability analysis is given which shows that our control law can guarantee the uniformly ultimate boundedness of the solution of the closed-loop system, and make the tracking error arbitrarily small.

Algorithms↗

PubMed2005

Iterative partial least squares with right-censored data analysis: a comparison to other dimension reduction techniques.

In the linear model with right-censored responses and many potential explanatory variables, regression parameter estimates may be unstable or, when the covariates outnumber the uncensored observations, not estimable. We propose an iterative algorithm for partial least squares, based on the Buckley-James estimating equation, to estimate the covariate effect and predict the response for a future subject with a given set of covariates. We use a leave-two-out cross-validation method for empirically selecting the number of components in the partial least-squares fit that approximately minimizes the error in estimating the covariate effect of a future observation. Simulation studies compare the methods discussed here with other dimension reduction techniques. Data from the AIDS Clinical Trials Group protocol 333 are used to motivate the methodology.

Anti-HIV Agents↗

PubMed2005

Energy generation from the CO oxidation-hydrogen production pathway in Rubrivivax gelatinosus.

When incubated in the presence of CO gas, Rubrivivax gelatinosus CBS induces a CO oxidation-H2 production pathway according to the stoichiometry CO + H2O --> CO2 + H2. Once induced, this pathway proceeds equally well in both light and darkness. When light is not present, CO can serve as the sole carbon source, supporting cell growth anaerobically with a cell doubling time of nearly 2 days. This observation suggests that the CO oxidation reaction yields energy. Indeed, new ATP synthesis was detected in darkness following CO additions to the gas phase of the culture, in contrast to the case for a control that received an inert gas such as argon. When the CO-to-H2 activity was determined in the presence of the electron transport uncoupler carbonyl-cyanide m-chlorophenylhydrazone (CCCP), the rate of H2 production from CO oxidation was enhanced nearly 40% compared to that of the control. Upon the addition of the ATP synthase inhibitor N,N'-dicyclohexylcarbodiimide (DCCD), we observed an inhibition of H2 production from CO oxidation which could be reversed upon the addition of CCCP. Collectively, these data strongly suggest that the CO-to-H2 reaction yields ATP driven by a transmembrane proton gradient, but the detailed mechanism of this reaction is not yet known. These findings encourage additional research aimed at long-term H2 production from gas streams containing CO.

Adenosine Triphosphate↗

PubMed2005

T2-prepared steady-state free precession blood oxygen level-dependent MR imaging of myocardial perfusion in a dog stenosis model.

PURPOSE: To assess the ability of a T2-prepared steady-state free precession blood oxygen level-dependent (BOLD) magnetic resonance (MR) imaging sequence to depict changes in myocardial perfusion during stress testing in a dog stenosis model. MATERIALS AND METHODS: Study was approved by the institutional Animal Care and Use Committee. A hydraulic occluder was placed in the left circumflex coronary artery (LCX) in 10 dogs. Adenosine was administered intravenously to increase coronary blood flow, and stenosis was achieved in the LCX with the occluder. A T2-prepared two-dimensional steady-state free precession sequence was used for BOLD imaging at a spatial resolution of 1.5 x 1.2 x 5.0 mm3, and first-pass perfusion images were acquired for visual comparison. Microspheres were injected to provide regional perfusion information. Mixed-effect regression analysis was performed to assess normalized MR signal intensity ratios and microsphere-measured perfusion differences. For the same data, 95% prediction intervals were calculated to determine the smallest perfusion change detectable. Means +/- standard deviations were calculated for myocardial regional comparison data. A two-tailed Student t test was used to determine if significant differences (P < .01) existed between different myocardial regions. RESULTS: Under maximal adenosine stress, MR clearly depicted stenotic regions and showed regional signal differences between the left anterior descending coronary artery (LAD)-fed myocardium and the stenosed LCX-fed myocardium. Visual comparisons with first-pass images were also excellent. Regional MR signal intensity differences between LAD and LCX-fed myocardium (1.24 +/- 0.08) were significantly different (P < .01) from differences between LAD and septal-fed myocardium (1.02 +/- 0.07), which was in agreement with microsphere-measured flow differences (LAD/LCX, 3.38 +/- 0.83; LAD/septal, 1.26 +/- 0.49). The linear mixed-effect regression model showed good correlation (R = 0.79) between MR differences and microsphere-measured flow differences. CONCLUSION: On T2-prepared steady-state free precession BOLD MR images in dogs, signal intensity differences were linearly related to flow differences in myocardium, with a high degree of correlation. SUPPLEMENTAL MATERIAL: radiology.rsnajnls.org/cgi/content/full/236/2/503/DC1

Animals↗

PubMed2005

[The implementation of sharing treatment planning system based on DICOM].

Based on DICOM, three DICOM objects of RT S. S, RT Plan, RT Image are designed to implement the information sharing of different TPS, and to implement the information exchanging and sharing of the radiotherapy planning systems (TPS) of different manufacturers. The information exchange of different TPS based on DICOM is feasible.

Computer Communication Networks↗

PubMed2005

Involvement of proteolytic activation of PKCdelta in cisplatin-induced apoptosis in human small cell lung cancer H69 cells.

Proteolytic activation of protein kinase C delta (PKCdelta) has been associated with apoptosis induced by the DNA damaging agent cisplatin. In cells undergoing apoptosis, caspase-3 cleaves PKCdelta at the site DMQD downward arrowN to generate a 40-kDa catalytic fragment. We have previously shown that the PKC signal transduction pathway regulates sensitivity of human small cell lung cancer H69 cells to cisplatin. In the present study, we have investigated if proteolytic activation of PKCdelta is essential for cisplatin-induced apoptosis in H69 cells. The caspase cleavage-resistant mutant PKCdelta (DMQA) was generated by mutating the aspartate residue at the site of proteolysis DMQD downward arrowN to alanine (D330A), and the wild-type and mutant PKCdelta were introduced into H69 cells. Cisplatin induced a substantial increase in PKCdelta catalytic fragment in H69 cells overexpressing PKCdelta (H69/delta, and the level of PKCdelta catalytic fragment in H69 cells expressing DMQA mutant (H69/DMQA) was equivalent to that in H69 cells. However, the cleavage of poly(ADP-ribose) polymerase (PARP), another substrate for caspase-3, was similar in cells overexpressing wild-type PKCdelta and DMQA mutant PKCdelta. The ability of cisplatin to induce mitochondrial depolarization and cell death was also equivalent among the cell lines tested. These results suggest that the proteolytic fragment of PKCdelta does not play a critical role in the induction of apoptosis in H69 cells.

Apoptosis↗

PubMed2005

[Identification and phylogenetic study of pathogenic bacteria causing ulcer disease of cultured Turbot (Scophthalmus maximus)].

An outbreak of ulcer disease of the cultured turbot Scophthalmus maximus L. occurred in an indoor farm in Haiyang, Shandong Province in the sweltering August of 2004 and caused significant mortality. At the beginning, infected turbots displayed sluggish swimming and anorexia. Several days later, the turbot eyes swelled, the fins and tail turned red, and the back gradually ulcerated. Dissection of the moribund fish showed that the ulcerative gills paled, the liver becamed bloodshot, the kidney and gallbladder swelled, the intestinal wall became filmy and bloodshot. The time course from appearance of disease signs to death lasted about a week. A dominant strain of bacteria, which was Gram-negative and short rod with single polar flagellum under electron microscope, was isolated from the diseased turbot and designated as H1. In artificial infection test, all fish of the experimental groups died in a week after intramuscularly injected with bacterial suspension, while the control group showed no signs in 10 d post-challenge. The moribund experimental fish had similar gross signs as the natural infected fish. The bacteria re-isolated from the challenged fish also had the same characteristics as H1, which proved that the isolate H1 was the pathogenic bacteria that triggered this ulcer disease. Different methods were used to identify the pathogenic bacteria. The identification result by API 20NE and API 20E system indicated that H1 was Aeromonas hydrophila, with 99% reliability and 61.5% respectively. While traditional biochemical identification revealed that H1 exhibited relatedness to Vibrio harveyi. In order to confirm the different result, a 1424 bp sequence of H1's 16S rDNA was amplified and compared with other Vibrio spp. in GenBank, homology analysis and phylogenetic study showed that H1 has the highest similarity to V. harveyi, with 99% identity. According to morphological features, physiological and biological characteristics and 16S rDNA homology comparison of the bacteria, the pathogenic bacteria were V. harveyi. Drugs sensitivity test showed that the pathogenic bacteria were highly sensitive to nitrofurantoinum and ceftriaxone sodium etc. This is the first report that V. harveyi was found as the pathogenic bacteria of cultured turbot in China. The research suggests that V. harveyi should be regarded as an important pathogen of turbot and can causes ulcer disease under conditions of high temperatures. Therefore, it is necessary to prevent against ulcer disease in culture turbot in summer.

Animals↗

PubMed2004

Annotations and functional analyses of the rice WRKY gene superfamily reveal positive and negative regulators of abscisic acid signaling in aleurone cells.

The WRKY proteins are a superfamily of regulators that control diverse developmental and physiological processes. This family was believed to be plant specific until the recent identification of WRKY genes in nonphotosynthetic eukaryotes. We have undertaken a comprehensive computational analysis of the rice (Oryza sativa) genomic sequences and predicted the structures of 81 OsWRKY genes, 48 of which are supported by full-length cDNA sequences. Eleven OsWRKY proteins contain two conserved WRKY domains, while the rest have only one. Phylogenetic analyses of the WRKY domain sequences provide support for the hypothesis that gene duplication of single- and two-domain WRKY genes, and loss of the WRKY domain, occurred in the evolutionary history of this gene family in rice. The phylogeny deduced from the WRKY domain peptide sequences is further supported by the position and phase of the intron in the regions encoding the WRKY domains. Analyses for chromosomal distributions reveal that 26% of the predicted OsWRKY genes are located on chromosome 1. Among the dozen genes tested, OsWRKY24, -51, -71, and -72 are induced by abscisic acid (ABA) in aleurone cells. Using a transient expression system, we have demonstrated that OsWRKY24 and -45 repress ABA induction of the HVA22 promoter-beta-glucuronidase construct, while OsWRKY72 and -77 synergistically interact with ABA to activate this reporter construct. This study provides a solid base for functional genomics studies of this important superfamily of regulatory genes in monocotyledonous plants and reveals a novel function for WRKY genes, i.e. mediating plant responses to ABA.

Abscisic Acid↗

PubMed2004

5-HT3A receptor subunits in the rat medial nucleus of the solitary tract: subcellular distribution and relation to the serotonin transporter.

The 5-hydroxytryptamine 3 (5HT3) receptor is a serotonin-gated ion channel implicated in reflex regulation of autonomic functions within the nucleus of the solitary tract (NTS). To determine the relevant sites for 5-HT3 receptor mediated transmission in this region, we used electron microscopic immunocytochemistry to examine the subcellular distribution of the 5HT3 receptor subunit A (5HT3A) in relation to the serotonin transporter (SERT) in the intermediate medial NTS (mNTS) of rat brain. The 5HT3A immunolabeling was detected in many axonal as well as somatodendritic and glial profiles. The axonal profiles included small axons and axon terminals in which the 5HT3A immunoreactivity was localized to membranes of synaptic vesicles and extrasynaptic plasma membranes. In dendrites and glia, the 5HT3A immunoreactivity was located on the plasma membranes or in association with membranous cytoplasmic organelles. The dendritic plasmalemmal 5HT3A labeling was prominent within and near excitatory-type synapses from terminals including those that resemble vagal afferents. The 5HT3A-labeled glial processes apposed 5HT3A-immunoreactive axonal and dendritic profiles, some of which also contained SERT. Terminals containing 5-HT3A and/or SERT were among those providing synaptic input to 5HT3A-labeled dendrites. Thus, 5HT3A has a subcellular distribution consistent with the involvement of 5-HT3 receptors in modulation of both presynaptic release and postsynaptic responses of mNTS neurons, some of which are serotonergic. The results further suggest that the neuronal as well as glial 5HT3 receptors can be activated by release of serotonin from presynaptic terminals or by diffusion facilitated by SERT distribution at a distant from the synapse.

Animals↗

PubMed2004

Use of e-Health services between 1999 and 2002: a growing digital divide.

OBJECTIVE: To evaluate the patterns of e-Health use over a four-year period and the characteristics of users. DESIGN: Longitudinal, population-based study (1999-2002) of members of a prepaid integrated delivery system. Available e-Health services included ordering prescription drug refills, scheduling appointments, and asking medical questions. MEASUREMENTS: Rates of known access to e-Health services, and of e-Health use each quarter. RESULTS: The number of members with known e-Health access increased from 51,336 (1.6%) in 1999 to 324,522 (9.3%), in 2002. The percentage of households in which at least one person in the household had access increased from 2.7% to 14.1%. Among the subjects with known access, the percentage of subjects that used e-Health at least once increased from 25.7% in 1999 to 36.2% in 2002. In the multivariate analysis, subjects who had a low expected clinical need, were nonwhite, or lived in low socioeconomic status (SES) neighborhoods were less likely to have used e-Health services in 2002. Disparities by race/ethnicity and SES persisted after controlling for access to e-Health and widened over time. CONCLUSION: Access to and use of e-Health services are growing rapidly. Use of these services appears to be greatest among persons with more medical need. The majority of subjects, however, do not use any e-Health services. More research is needed to determine potential reasons for disparities in e-Health use by race/ethnicity and SES as well as the implications of these disparities on clinical outcomes.

Adolescent↗