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PubMed2006

Evaluating telemedicine: a focus on patient pathways.

Evaluations of telemedicine have sought to assess various measures of effectiveness (e.g., diagnostic accuracy), efficiency (e.g., cost), and engagement (e.g., patient satisfaction) to determine its success. Few studies, however, have looked at evaluating the organizational impact of telemedicine, which involves technology and process changes that affect the way that it is used and accepted by patients and clinicians alike. This study reviews and discusses the conceptual issues in telemedicine research and proposes a fresh approach for evaluating telemedicine. First, we advance a patient pathway perspective, as most of the existing studies view telemedicine as a support to a singular rather than multiple aspects of a health care process. Second, to conceptualize patient pathways and understand how telemedicine impacts upon them, we propose simulation as a tool to enhance understanding of the traditional and telemedicine patient pathway.

Computer Simulation↗
PubMedDate not supplied

Pathways for head and neck surgery: a patient-education tool.

Surgical treatment for head and neck cancer includes a variety of complex operative procedures. Patients scheduled for these operations often are presented with overwhelming amounts of information. Even after participating in the multidisciplinary, preoperative teaching process, they may be unable to fully comprehend the treatment plan. Pathways for head and neck surgery were designed to facilitate the patient- and family-education process and assist the patient in navigating through the surgical experience. This article discusses head and neck surgery pathway development, implementation, and outcome evaluation.

Critical Pathways↗
PubMedDate not supplied

Pathways for continence care: development of the pathways.

This article is the second in a series of three covering a project into the use of care pathways for continence care undertaken by the authors. Loddon NHS Trust, Wiltshire and Swindon Healthcare NHS Trust and Salisbury Healthcare NHS Trust collaborated and supported their continence advisers in moving from financially driven assessment data to writing evidence-based care pathways and supporting patient information. The first article (Vol 9(9): 590-6) described the issues facing the continence advisers and the background to their decision to use full evidence-based care pathways. It also gave the results of an audit demonstrating that high quality equitable continence care was not reaching each patient. This article covers the literature search and the problems encountered in the setting up of a database and the development of a generic pathway, a symptom profile and specific pathways. It describes how each pathway evolved and was underpinned with the relevant evidence. It further describes the supporting information and design problems. Finally, it gives information on piloting the care pathways.

Critical Pathways↗
PubMed1999

Not resting on its laurels, Sentara taps data analysis tool to fine-tune pathways.

Artificial intelligence data analysis leads health care system to fine-tune and improve new clinical pathways. Sentara Health Care in Norfolk, VA, developed a host of new clinical protocols in recent years, but instead of sitting back and enjoying initial improved outcomes and cost savings, it went the extra mile to enhance those pathways using a sophisticated data analysis tool.

Artificial Intelligence↗
PubMed1999

Pathways bring dramatic clinical results.

Although physicians at Good Samaritan Health System in Kearney, NE, first offered stiff resistance to case managers' efforts to implement a clinical pathway program, efforts to educate the physicians about the benefits of pathways have led to a turn-around in which physicians now are asking the director of case management to create even more pathways. One key step in promoting the pathways was to create a reporting profile capable of evaluating clinical pathways. In addition, the hospital produced a video for each pathway that describes the patient's care from preadmission through discharge. Most significantly, case managers at Good Samaritan avoided creating an adversarial relationship with physicians in the system. They dodged charges of pathways being "cookbook medicine" by establishing a system in which pathways are not automatically applied; physicians have to write an order for a patient to be placed on a pathway.

Attitude of Health Personnel↗
PubMed2004

The alternative activation pathway and complement component C3 are critical for a protective immune response against Pseudomonas aeruginosa in a murine model of pneumonia.

Pseudomonas aeruginosa is a leading cause of hospital-acquired pneumonia, and approximately 80% of patients with cystic fibrosis are infected with this bacterium. To investigate the overall role of complement and the complement activation pathways in the host defense against P. aeruginosa pulmonary infection, we challenged C3-, C4-, and factor B-deficient mice with P. aeruginosa via intranasal inoculation. In these studies, C3(-/-) mice had a higher mortality rate than C3(+/+) mice. Factor B(-/-) mice, but not C4(-/-) mice, infected with P. aeruginosa had a mortality rate similar to that of C3(-/-) mice, indicating that in this model the alternative pathway of complement activation is required for the host defense against Pseudomonas infection. C3(-/-) mice had 6- to 7-fold more bacteria in the lungs and 48-fold more bacteria in the blood than did C3(+/+) mice at 24 h postinfection. In vitro, phagocytic cells from C3(+/+) or C3(-/-) mice exhibited a decreased ability to bind and/or ingest P. aeruginosa in the presence of C3-deficient serum compared to phagocytic cells in the presence of serum with sufficient C3. C3(-/-) mice displayed a significant increase in neutrophils in the lungs and had higher levels of interleukin-1beta (IL-1beta), IL-6, IL-10, KC, and MIP-2 in the lungs at 24 h postinfection than did C3(+/+) mice. Collectively, these results indicate that complement activation by the alternative pathway is critical for the survival of mice infected with P. aeruginosa and that the protection provided by complement is at least in part due to C3-mediated opsonization and phagocytosis of P. aeruginosa.

Animals↗
PubMed2006

Crystal structure of a beta-catenin/BCL9/Tcf4 complex.

The canonical Wnt pathway plays critical roles in embryonic development, stem cell growth, and tumorigenesis. Stimulation of the Wnt pathway leads to the association of beta-catenin with Tcf and BCL9 in the nucleus, resulting in the transactivation of Wnt target genes. We have determined the crystal structure of a beta-catenin/BCL9/Tcf-4 triple complex at 2.6 A resolution. Our studies reveal that the beta-catenin binding site of BCL9 is distinct from that of most other beta-catenin partners and forms a good target for developing drugs that block canonical Wnt/beta-catenin signaling. The BCL9 beta-catenin binding domain (CBD) forms an alpha helix that binds to the first armadillo repeat of beta-catenin, which can be mutated to prevent beta-catenin binding to BCL9 without affecting cadherin or alpha-catenin binding. We also demonstrate that beta-catenin Y142 phosphorylation, which has been proposed to regulate BCL9-2 binding, does not directly affect the interaction of beta-catenin with either BCL9 or BCL9-2.

Amino Acid Sequence↗
PubMed1999

Mouse suppressor of fused is a negative regulator of sonic hedgehog signaling and alters the subcellular distribution of Gli1.

The Hedgehog (Hh) signaling pathway has critical functions during embryogenesis of both invertebrate and vertebrate species [1]; defects in this pathway in humans can cause developmental disorders as well as neoplasia [2]. Although the Gli1, Gli2, and Gli3 zinc finger proteins are known to be effectors of Hh signaling in vertebrates, the mechanisms regulating activity of these transcription factors remain poorly understood [3] [4]. In Drosophila, activity of the Gli homolog Cubitus interruptus (Ci) is likely to be modulated by its interaction with a cytoplasmic complex containing several other proteins [5] [6], including Costal2, Fused (Fu), and Suppressor of fused (Su(fu)), the last of which has been shown to interact directly with Ci [7]. We have cloned mouse Suppressor of fused (mSu(fu)) and detected its 4.5 kb transcript throughout embryogenesis and in several adult tissues. In cultured cells, mSu(fu) overexpression inhibited transcriptional activation mediated by Sonic hedgehog (Shh), Gli1 and Gli2. Co-immunoprecipitation of epitope-tagged proteins indicated that mSu(fu) interacts with Gli1, Gli2, and Gli3, and that the inhibitory effects of mSu(fu) on Gli1's transcriptional activity were mediated through interactions with both amino- and carboxy-terminal regions of Gli1. Gli1 was localized primarily to the nucleus of both HeLa cells and the Shh-responsive cell line MNS-70; co-expression with mSu(fu) resulted in a striking increase in cytoplasmic Gli1 immunostaining. Our findings indicate that mSu(fu) can function as a negative regulator of Shh signaling and suggest that this effect is mediated by interaction with Gli transcription factors.

Amino Acid Sequence↗
PubMed2001

Inhibition of Tcf3 binding by I-mfa domain proteins.

We have determined that I-mfa, an inhibitor of several basic helix-loop-helix (bHLH) proteins, and XIC, a Xenopus ortholog of human I-mf domain-containing protein that shares a highly conserved cysteine-rich C-terminal domain with I-mfa, inhibit the activity and DNA binding of the HMG box transcription factor XTcf3. Ectopic expression of I-mfa or XIC in early Xenopus embryos inhibited dorsal axis specification, the expression of the Tcf3/beta-catenin-regulated genes siamois and Xnr3, and the ability of beta-catenin to activate reporter constructs driven by Lef/Tcf binding sites. I-mfa domain proteins can regulate both the Wnt signaling pathway and a subset of bHLH proteins, possibly coordinating the activities of these two critical developmental pathways.

Amino Acid Sequence↗
PubMed2004

Mechanisms of paclitaxel-induced apoptosis in an ovarian cancer cell line and its paclitaxel-resistant clone.

BACKGROUND: To understand the complicated network of paclitaxel (PTX)-induced apoptosis pathways and to elucidate mechanisms of drug resistance in ovarian cancer, we looked at PTX-induced apoptosis by using cDNA microarray. We also quantitated the changes in apoptosis-related proteins in the process of apoptosis. METHODS: An ovarian cancer cell line KF, and its PTX-resistant clone KFTX, were treated with PTX or carboplatin (CBDCA). After exposure to PTX or CBDCA, the induction of apoptosis was examined by internucleosomal DNA fragmentation. Changes in mRNA expression after 12 h of exposure to PTX were studied using cDNA microarray and RT-PCR. Changes in P53 and Bcl-2 levels were also measured over 24 h by ELISA. RESULTS: With increased doses of PTX or CBDCA, an increase in apoptosis was noted in both cell lines. cDNA microarray revealed that PTX treatment upregulated expression of caspase 1, 2, 3, 4, 6, 9, 10, their activator apaf-1, and stress reaction-related genes, gadd34, gadd153 in KF, although most of them were unchanged or downregulated in KFTX. bag-1 and hsc70 were markedly upregulated in KFTX. p53 and bcl-2 were not upregulated in either cell line. Results from protein studies also supported the cDNA microarray data. CONCLUSIONS: p53-independent mitochondrial pathways and stress-reaction-induced pathways play critical roles in PTX-induced apoptosis in ovarian cancer cells. Suppression of those pathways and upregulation of bag-1 and hsp-70 played an important role in acquiring resistance to PTX.

Antineoplastic Agents, Phytogenic↗