3750 S Jones Blvd Ste 120
Las Vegas NV 89103
Medical School: Other - 2002
Accepts Medicare: Yes
Participates In eRX: Yes
Participates In PQRS: No
Participates In EHR: Yes
License #: 11544
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Dr. Julie Wu is associated with these group practices
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Allowed By Medicare
|HCPCS Code:99204||Description:Office/outpatient visit new||Average Price:$280.00||Average Price Allowed
|HCPCS Code:99203||Description:Office/outpatient visit new||Average Price:$188.57||Average Price Allowed
|HCPCS Code:99214||Description:Office/outpatient visit est||Average Price:$185.42||Average Price Allowed
|HCPCS Code:99348||Description:Home visit est patient||Average Price:$152.00||Average Price Allowed
|HCPCS Code:99213||Description:Office/outpatient visit est||Average Price:$127.69||Average Price Allowed
|HCPCS Code:99308||Description:Nursing fac care subseq||Average Price:$114.58||Average Price Allowed
|HCPCS Code:90662||Description:Flu vacc prsv free inc antig||Average Price:$60.00||Average Price Allowed
|HCPCS Code:G0008||Description:Admin influenza virus vac||Average Price:$53.00||Average Price Allowed
HCPCS Code Definitions
- Administration of influenza virus vaccine
- Office or other outpatient visit for the evaluation and management of a new patient, which requires these 3 key components: A comprehensive history; A comprehensive examination; Medical decision making of moderate complexity. Counseling and/or coordination of care with other physicians, other qualified health care professionals, or agencies are provided consistent with the nature of the problem(s) and the patient's and/or family's needs. Usually, the presenting problem(s) are of moderate to high severity. Typically, 45 minutes are spent face-to-face with the patient and/or family.
- Home visit for the evaluation and management of an established patient, which requires at least 2 of these 3 key components: An expanded problem focused interval history; An expanded problem focused examination; Medical decision making of low complexity. Counseling and/or coordination of care with other physicians, other qualified health care professionals, or agencies are provided consistent with the nature of the problem(s) and the patient's and/or family's needs. Usually, the presenting problem(s) are of low to moderate severity. Typically, 25 minutes are spent face-to-face with the patient and/or family.
- Office or other outpatient visit for the evaluation and management of a new patient, which requires these 3 key components: A detailed history; A detailed examination; Medical decision making of low complexity. Counseling and/or coordination of care with other physicians, other qualified health care professionals, or agencies are provided consistent with the nature of the problem(s) and the patient's and/or family's needs. Usually, the presenting problem(s) are of moderate severity. Typically, 30 minutes are spent face-to-face with the patient and/or family.
- Subsequent nursing facility care, per day, for the evaluation and management of a patient, which requires at least 2 of these 3 key components: An expanded problem focused interval history; An expanded problem focused examination; Medical decision making of low complexity. Counseling and/or coordination of care with other physicians, other qualified health care professionals, or agencies are provided consistent with the nature of the problem(s) and the patient's and/or family's needs. Usually, the patient is responding inadequately to therapy or has developed a minor complication. Typically, 15 minutes are spent at the bedside and on the patient's facility floor or unit.
- Office or other outpatient visit for the evaluation and management of an established patient, which requires at least 2 of these 3 key components: An expanded problem focused history; An expanded problem focused examination; Medical decision making of low complexity. Counseling and coordination of care with other physicians, other qualified health care professionals, or agencies are provided consistent with the nature of the problem(s) and the patient's and/or family's needs. Usually, the presenting problem(s) are of low to moderate severity. Typically, 15 minutes are spent face-to-face with the patient and/or family.
- Office or other outpatient visit for the evaluation and management of an established patient, which requires at least 2 of these 3 key components: A detailed history; A detailed examination; Medical decision making of moderate complexity. Counseling and/or coordination of care with other physicians, other qualified health care professionals, or agencies are provided consistent with the nature of the problem(s) and the patient's and/or family's needs. Usually, the presenting problem(s) are of moderate to high severity. Typically, 25 minutes are spent face-to-face with the patient and/or family.
Medical Malpractice Cases
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Plastic And Reconstructive Surgery
Cardiovascular Disease (Cardiology)
Cardiovascular Disease (Cardiology)
*These referrals represent the top 10 that Dr. Wu has made to other doctors
Emerging differential roles of the pRb tumor suppressor in trichodysplasia spinulosa-associated polyomavirus and Merkel cell polyomavirus pathogeneses. - Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology
Merkel cell carcinoma (MCC) and trichodysplasia spinulosa (TS) are two proliferative cutaneous diseases caused by the Merkel cell polyomavirus (MCPyV) and trichodysplasia spinulosa-associated polyomavirus (TSPyV) respectively. Recently, studies have elucidated a key role of the small tumor (sT) antigen in the proliferative pathogenic mechanisms of MCPyV and likely TSPyV. While both sT antigens have demonstrated a capacity in regulating cellular pathways, it remains unknown whether MCPyV and TSPyV sT antigens contribute similarly or differentially to cell proliferation.The present study aims to explore the proliferative potential of MCPyV and TSPyV sT antigens by investigating their regulatory effects on the retinoblastoma protein (pRb) tumor suppressor.Inducible cell lines expressing MCPyV sT or TSPyV sT were created using a lentiviral packaging system. Cellular proteins were extracted and subjected to SDS-PAGE followed by Western blot detection and densitometric analysis.Expression of TSPyV sT markedly enhanced the phosphorylation of pRb in Western blot experiments. In contrast, expression of MCPyV sT did not alter pRb phosphorylation under the same experimental conditions. Densitometric analysis revealed that TSPyV sT antigen expression nearly doubled the ratio of phosphorylated to total pRb (P<0.001, Student's T-test), while MCPyV sT antigen expression did not cause significant change in pRb phosphorylation status.Given that hyperphosphorylation of pRb is associated with dysregulation of the cell cycle, S-phase induction, and increased cell proliferation, our findings support an important role of TSPyV-mediated pRb deactivation in the development of TS. The observation that the pRb tumor suppressor is inactivated by TSPyV sT but not MCPyV sT provides further insights into the distinct pathobiological mechanisms of MCC and TS.Copyright Â© 2016 Elsevier B.V. All rights reserved.
ProEx(â„¢) C is a useful ancillary study for grading anal intraepithelial neoplasia alone and in combination with other biomarkers. - APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
Anal intraepithelial neoplasia (AIN) is a precursor to invasive anal squamous cell carcinoma. Histologic evaluation is hampered by intra- and interobserver variability. Various biomarkers have been investigated to improve the accuracy and reproducibility of diagnosis and grading, but interpretation can be challenging. ProEx(â„¢) C is an antibody cocktail for proteins upregulated in cervical intraepithelial neoplasia. This study investigated ProEx(â„¢) C's role alone and with p16 and Ki-67 in the diagnosis and grading of AIN. Sixty-seven anal tissue samples (22 AIN I, 25 AIN II/III, and 20 non-dysplastic) were stained for ProEx(â„¢) C, Ki-67, and p16. Staining patterns were recorded and correlated with morphologic diagnoses. Considering AIN II/III vs I, full-thickness ProEx(â„¢) C staining was more frequent in AIN II/III (p = 0.0373), and showed the highest sensitivity of the biomarkers. In combination with Ki-67, sensitivity was lower, but specificity for AIN II/III rose to 83%. For differentiating non-dysplasia from AIN I, negative ProEx(â„¢) C staining correlated with non-dysplasia (p < 0.0001) and had the highest sensitivity (90%). In combination with Ki-67, sensitivity dropped to 80%, but specificity was high (96%). ProEx(â„¢) C is useful for diagnosing and grading AIN, performing as well or better than other markers at identifying AIN II/III and non-dysplastic epithelium.Â© 2015 APMIS. Published by John Wiley & Sons Ltd.
Effectiveness of a novel interactive health care education tool on clinical outcomes and quality of life in acne patients: A randomized controlled pilot study. - The Journal of dermatological treatment
We developed an Internet-based education tool (My Personalized Application for health Care Education, MyPACE) to promote patient comprehension about acne.To determine if MyPACE improves clinical outcomes and quality of life in acne patients.Modeling the spaced education approach, 50 participants received weekly multiple-choice questions for 12 weeks. Those randomized to the intervention group received acne-related questions, while those in the control group received non-dermatologic health-related questions. Acne lesion counts and Dermatology Life Quality Index (DLQI) scores were recorded at initial enrollment and at 12 weeks.Within-group analysis for the intervention group showed a significant mean change in inflammatory and non-inflammatory acne lesions per person (-3.2â€‰Â±â€‰1.3, pâ€‰=â€‰0.0219; -4.4â€‰Â±â€‰1.8, pâ€‰=â€‰0.0267, respectively). The control group only demonstrated a significant mean change in inflammatory lesions (-2.8â€‰Â±â€‰0.80, pâ€‰=â€‰0.0040). Both groups had statistically significant improvement in DLQI score. Compared with participants in the control group, those receiving acne-related questions experienced greater improvement in clinical outcomes and quality of life.The small sample size limited our ability to detect statistically significant differences.Internet-based, disease-specific, spaced education tools may be more effective than non-targeted tools for improving clinical outcomes and quality of life.
Homer3 regulates the establishment of neutrophil polarity. - Molecular biology of the cell
Most chemoattractants rely on activation of the heterotrimeric G-protein GÎ±i to regulate directional cell migration, but few links from GÎ±i to chemotactic effectors are known. Through affinity chromatography using primary neutrophil lysate, we identify Homer3 as a novel GÎ±i2-binding protein. RNA interference-mediated knockdown of Homer3 in neutrophil-like HL-60 cells impairs chemotaxis and the establishment of polarity of phosphatidylinositol 3,4,5-triphosphate (PIP3) and the actin cytoskeleton, as well as the persistence of the WAVE2 complex. Most previously characterized proteins that are required for cell polarity are needed for actin assembly or activation of core chemotactic effectors such as the Rac GTPase. In contrast, Homer3-knockdown cells show normal magnitude and kinetics of chemoattractant-induced activation of phosphoinositide 3-kinase and Rac effectors. Chemoattractant-stimulated Homer3-knockdown cells also exhibit a normal initial magnitude of actin polymerization but fail to polarize actin assembly and intracellular PIP3 and are defective in the initiation of cell polarity and motility. Our data suggest that Homer3 acts as a scaffold that spatially organizes actin assembly to support neutrophil polarity and motility downstream of GPCR activation.Â© 2015 Wu etÂ al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attributionâ€“Noncommercialâ€“Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).
Metabolomics in psoriatic disease: pilot study reveals metabolite differences in psoriasis and psoriatic arthritis. - F1000Research
While "omics" studies have advanced our understanding of inflammatory skin diseases, metabolomics is mostly an unexplored field in dermatology.We sought to elucidate the pathogenesis of psoriatic diseases by determining the differences in metabolomic profiles among psoriasis patients with or without psoriatic arthritis and healthy controls.We employed a global metabolomics approach to compare circulating metabolites from patients with psoriasis, psoriasis and psoriatic arthritis, and healthy controls.Study participants were recruited from the general community and from the Psoriasis Clinic at the University of California Davis in United States.We examined metabolomic profiles using blood serum samples from 30 patients age and gender matched into three groups: 10 patients with psoriasis, 10 patients with psoriasis and psoriatic arthritis and 10 control participants. Main outcome(s) and measures(s): Metabolite levels were measured calculating the mean peak intensities from gas chromatography time-of-flight mass spectrometry.Multivariate analyses of metabolomics profiles revealed altered serum metabolites among the study population. Compared to control patients, psoriasis patients had a higher level of alpha ketoglutaric acid (Pso: 288 Â± 88;209 Â± 69; p=0.03), a lower level of asparagine (Pso: 5460 Â± 980;7260 Â± 2100; p=0.02), and a lower level of glutamine (Pso: 86000 Â± 20000;111000 Â± 27000; p=0.02). Compared to control patients, patients with psoriasis and psoriatic arthritis had increased levels of glucuronic acid (Pso + PsA: 638 Â± 250;347 Â± 61; p=0.001). Compared to patients with psoriasis alone, patients with both psoriasis and psoriatic arthritis had a decreased level of alpha ketoglutaric acid (Pso + PsA: 186 Â± 80; Pso: 288 Â± 88; p=0.02) and an increased level of lignoceric acid (Pso + PsA: 442 Â± 280; Pso: 214 Â± 64; p=0.02).The metabolite differences help elucidate the pathogenesis of psoriasis and psoriatic arthritis and they may provide insights for therapeutic development.
Smoking cessation is associated with decreased mortality and improved amputation-free survival among patients with symptomatic peripheral artery disease. - Journal of vascular surgery
Although smoking cessation is recommended for all patients with peripheral artery disease, there are little data regarding the prevalence of smoking among patients at the time of angiography or the effect of smoking cessation on clinical outcomes.Consecutive patients with claudication or critical limb ischemia who underwent peripheral angiography from 2006 to 2013 were included in an observational cohort analysis. Smoking status was assessed at the time of angiography and during follow-up clinic visits. Kaplan-Meier analysis was used to assess the relationship between smoking cessation, mortality, and amputation-free survival.Among 739 patients (423 men and 316 women; mean age, 60 Â± 12 years), 204 (28%) remained active smokers at the time of lower extremity angiography. At the time of angiography, the mean number of cigarettes smoked per day was 16 Â± 10, and the mean pack-years was 40 Â± 25. During the course of the subsequent year, 61 patients (30%) successfully quit smoking and maintained continued abstinence. Baseline medication use between groups did not differ significantly. The mean ankle-brachial index was also similar for quitters vs nonquitters (0.53 Â± 24 vs 0.49 Â± 0.22; P = .3). During follow-up to 5 years, patients who quit smoking had significantly lower all-cause mortality (14% vs 31%; hazard ratio, 0.40; 95% confidence interval, 0.18-0.90) and improved amputation-free survival (81% vs 60%; hazard ratio, 0.43, 95% confidence interval, 0.22-0.86) compared with patients who continued smoking, with most of the difference driven by reduced mortality among patients who quit smoking. The findings remained significant on multivariable analysis.Approximately one-third of active smokers with peripheral artery disease successfully quit smoking â‰¤ 1 year after lower extremity angiography. Patients who quit smoking have lower mortality and improved amputation-free survival compared with patients who continue smoking.Published by Elsevier Inc.
Interplay between brain stem angiotensins and monocyte chemoattractant protein-1 as a novel mechanism for pressor response after ischemic stroke. - Neurobiology of disease
Pressor response after stroke commonly leads to early death or susceptibility to stroke recurrence, and detailed mechanisms are still lacking. We assessed the hypothesis that the renin-angiotensin system contributes to pressor response after stroke by differential modulation of the pro-inflammatory chemokine monocyte chemoattractant protein-1 (MCP-1) in the rostral ventrolateral medulla (RVLM), a key brain stem site that maintains blood pressure. We also investigated the beneficial effects of a novel renin inhibitor, aliskiren, against stroke-elicited pressor response. Experiments were performed in male adult Sprague-Dawley rats. Stroke induced by middle cerebral artery occlusion elicited significant pressor response, accompanied by activation of angiotensin II (Ang II)/type I receptor (AT1R) and AT2R signaling, depression of Ang-(1-7)/MasR and Ang IV/AT4R cascade, alongside augmentation of MCP-1/C-C chemokine receptor 2 (CCR2) signaling and neuroinflammation in the RVLM. Stroke-elicited pressor response was significantly blunted by antagonism of AT1R, AT2R or MCP-1/CCR2 signaling, and eliminated by applying Ang-(1-7) or Ang IV into the RVLM. Furthermore, stroke-activated MCP-1/CCR2 signaling was enhanced by AT1R and AT2R activation, and depressed by Ang-(1-7)/MasR and Ang IV/AT4R cascade. Aliskiren inhibited stroke-elicited pressor response via downregulating MCP-1/CCR2 activity and reduced neuroinflammation in the RVLM; these effects were potentiated by Ang-(1-7) or Ang IV. We conclude that whereas Ang II/AT1R or Ang II/AT2R signaling in the brain stem enhances, Ang-(1-7)/MasR or Ang IV/AT4R antagonizes pressor response after stroke by differential modulations of MCP-1 in the RVLM. Furthermore, combined administration of aliskiren and Ang-(1-7) or Ang IV into the brain stem provides more effective amelioration of stroked-induced pressor response.Copyright Â© 2014 Elsevier Inc. All rights reserved.
Metabolomic analysis using porcine skin: a pilot study of analytical techniques. - Dermatology online journal
Metabolic byproducts serve as indicators of the chemical processes and can provide valuable information on pathogenesis by measuring the amplified output. Standardized techniques for metabolome extraction of skin samples serve as a critical foundation to this field but have not been developed.We sought to determine the optimal cell lysage techniques for skin sample preparation and to compare GC-TOF-MS and UHPLC-QTOF-MS for metabolomic analysis.Using porcine skin samples, we pulverized the skin via various combinations of mechanical techniques for cell lysage. After extraction, the samples were subjected to GC-TOF-MS and/or UHPLC-QTOF-MS.Signal intensities from GC-TOF-MS analysis showed that ultrasonication (2.7x107) was most effective for cell lysage when compared to mortar-and-pestle (2.6x107), ball mill followed by ultrasonication (1.6x107), mortar-and-pestle followed by ultrasonication (1.4x107), and homogenization (trial 1: 8.4x106; trial 2: 1.6x107). Due to the similar signal intensities, ultrasonication and mortar-and-pestle were applied to additional samples and subjected to GC-TOF-MS and UHPLC-QTOF-MS. Ultrasonication yielded greater signal intensities than mortar-and-pestle for 92% of detected metabolites following GC-TOF-MS and for 68% of detected metabolites following UHPLC-QTOF-MS.Overall, ultrasonication is the preferred method for efficient cell lysage of skin tissue for both metabolomic platforms. With standardized sample preparation, metabolomic analysis of skin can serve as a powerful tool in elucidating underlying biological processes in dermatological conditions.
Itk-mediated integration of T cell receptor and cytokine signaling regulates the balance between Th17 and regulatory T cells. - The Journal of experimental medicine
A proper balance between Th17 and T regulatory cells (Treg cells) is critical for generating protective immune responses while minimizing autoimmunity. We show that the Tec family kinase Itk (IL2-inducible T cell kinase), a component of T cell receptor (TCR) signaling pathways, influences this balance by regulating cross talk between TCR and cytokine signaling. Under both Th17 and Treg cell differentiation conditions, Itk(-/-) CD4(+) T cells develop higher percentages of functional FoxP3(+) cells, associated with increased sensitivity to IL-2. Itk(-/-) CD4(+) T cells also preferentially develop into Treg cells in vivo. We find that Itk-deficient T cells exhibit reduced TCR-induced phosphorylation of mammalian target of rapamycin (mTOR) targets, accompanied by downstream metabolic alterations. Surprisingly, Itk(-/-) cells also exhibit reduced IL-2-induced mTOR activation, despite increased STAT5 phosphorylation. We demonstrate that in wild-type CD4(+) T cells, TCR stimulation leads to a dose-dependent repression of Pten. However, at low TCR stimulation or in the absence of Itk, Pten is not effectively repressed, thereby uncoupling STAT5 phosphorylation and phosphoinositide-3-kinase (PI3K) pathways. Moreover, Itk-deficient CD4(+) T cells show impaired TCR-mediated induction of Myc and miR-19b, known repressors of Pten. Our results demonstrate that Itk helps orchestrate positive feedback loops integrating multiple T cell signaling pathways, suggesting Itk as a potential target for altering the balance between Th17 and Treg cells.
Decision aids for people facing health treatment or screening decisions. - The Cochrane database of systematic reviews
Decision aids are intended to help people participate in decisions that involve weighing the benefits and harms of treatment options often with scientific uncertainty.To assess the effects of decision aids for people facing treatment or screening decisions.For this update, we searched from 2009 to June 2012 in MEDLINE; CENTRAL; EMBASE; PsycINFO; and grey literature. Cumulatively, we have searched each database since its start date including CINAHL (to September 2008).We included published randomized controlled trials of decision aids, which are interventions designed to support patients' decision making by making explicit the decision, providing information about treatment or screening options and their associated outcomes, compared to usual care and/or alternative interventions. We excluded studies of participants making hypothetical decisions.Two review authors independently screened citations for inclusion, extracted data, and assessed risk of bias. The primary outcomes, based on the International Patient Decision Aid Standards (IPDAS), were:A) 'choice made' attributes;B) 'decision-making process' attributes.Secondary outcomes were behavioral, health, and health-system effects. We pooled results using mean differences (MD) and relative risks (RR), applying a random-effects model.This update includes 33 new studies for a total of 115 studies involving 34,444 participants. For risk of bias, selective outcome reporting and blinding of participants and personnel were mostly rated as unclear due to inadequate reporting. Based on 7 items, 8 of 115 studies had high risk of bias for 1 or 2 items each.Of 115 included studies, 88 (76.5%) used at least one of the IPDAS effectiveness criteria: A) 'choice made' attributes criteria: knowledge scores (76 studies); accurate risk perceptions (25 studies); and informed value-based choice (20 studies); and B) 'decision-making process' attributes criteria: feeling informed (34 studies) and feeling clear about values (29 studies).A) Criteria involving 'choice made' attributes:Compared to usual care, decision aids increased knowledge (MD 13.34 out of 100; 95% confidence interval (CI) 11.17 to 15.51; n = 42). When more detailed decision aids were compared to simple decision aids, the relative improvement in knowledge was significant (MD 5.52 out of 100; 95% CI 3.90 to 7.15; n = 19). Exposure to a decision aid with expressed probabilities resulted in a higher proportion of people with accurate risk perceptions (RR 1.82; 95% CI 1.52 to 2.16; n = 19). Exposure to a decision aid with explicit values clarification resulted in a higher proportion of patients choosing an option congruent with their values (RR 1.51; 95% CI 1.17 to 1.96; n = 13).B) Criteria involving 'decision-making process' attributes:Decision aids compared to usual care interventions resulted in:a) lower decisional conflict related to feeling uninformed (MD -7.26 of 100; 95% CI -9.73 to -4.78; n = 22) and feeling unclear about personal values (MD -6.09; 95% CI -8.50 to -3.67; n = 18);b) reduced proportions of people who were passive in decision making (RR 0.66; 95% CI 0.53 to 0.81; n = 14); andc) reduced proportions of people who remained undecided post-intervention (RR 0.59; 95% CI 0.47 to 0.72; n = 18).Decision aids appeared to have a positive effect on patient-practitioner communication in all nine studies that measured this outcome. For satisfaction with the decision (n = 20), decision-making process (n = 17), and/or preparation for decision making (n = 3), those exposed to a decision aid were either more satisfied, or there was no difference between the decision aid versus comparison interventions. No studies evaluated decision-making process attributes for helping patients to recognize that a decision needs to be made, or understanding that values affect the choice.C) Secondary outcomes Exposure to decision aids compared to usual care reduced the number of people of choosing major elective invasive surgery in favour of more conservative options (RR 0.79; 95% CI 0.68 to 0.93; n = 15). Exposure to decision aids compared to usual care reduced the number of people choosing to have prostate-specific antigen screening (RR 0.87; 95% CI 0.77 to 0.98; n = 9). When detailed compared to simple decision aids were used, fewer people chose menopausal hormone therapy (RR 0.73; 95% CI 0.55 to 0.98; n = 3). For other decisions, the effect on choices was variable.The effect of decision aids on length of consultation varied from 8 minutes shorter to 23 minutes longer (median 2.55 minutes longer) with 2 studies indicating statistically-significantly longer, 1 study shorter, and 6 studies reporting no difference in consultation length. Groups of patients receiving decision aids do not appear to differ from comparison groups in terms of anxiety (n = 30), general health outcomes (n = 11), and condition-specific health outcomes (n = 11). The effects of decision aids on other outcomes (adherence to the decision, costs/resource use) were inconclusive.There is high-quality evidence that decision aids compared to usual care improve people's knowledge regarding options, and reduce their decisional conflict related to feeling uninformed and unclear about their personal values. There is moderate-quality evidence that decision aids compared to usual care stimulate people to take a more active role in decision making, and improve accurate risk perceptions when probabilities are included in decision aids, compared to not being included. There is low-quality evidence that decision aids improve congruence between the chosen option and the patient's values.New for this updated review is further evidence indicating more informed, values-based choices, and improved patient-practitioner communication. There is a variable effect of decision aids on length of consultation. Consistent with findings from the previous review, decision aids have a variable effect on choices. They reduce the number of people choosing discretionary surgery and have no apparent adverse effects on health outcomes or satisfaction. The effects on adherence with the chosen option, cost-effectiveness, use with lower literacy populations, and level of detail needed in decision aids need further evaluation. Little is known about the degree of detail that decision aids need in order to have a positive effect on attributes of the choice made, or the decision-making process.
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3750 S Jones Blvd Ste 120 Las Vegas, NV 89103
5419 W. Tropicana Ave., Apt.#2702
6803 W Tropicana Ave Ste #100