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Results for “Critical Pathways”

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At least 1,333 records · Page 74Linked to original sources
PubMed1999

Development of a renal transplant clinical pathway: one hospital's journey.

Mounting pressures to resolve multiple challenges related to quality, cost, and access in a resource-driven, customer-focused health care environment have compelled clinicians to develop innovative strategies to provide cost-effective, state-of-the-art care. Targeted patient groups include those associated with high cost, high volume, or high resource use. Patients undergoing renal transplantation fall into one or more of these categories. Recently, the management of patients with end-stage renal disease (ESRD) has come under national focus, as evidenced by the fact that Health Care Financing Administration (HCFA) has commissioned an ESRD managed care demonstration project. The purpose of this article is to describe how one case management tool--the clinical pathway--can be used to decrease costs and improve outcomes associated with renal transplantation. This discussion will include a review of the origins and components of clinical pathways and a description of how one institution developed, implemented, evaluated, and refined a renal transplantation clinical pathway.

Case Management↗
PubMed1997

Development and implementation of clinical pathways for stroke on a multihospital basis.

This study describes the development and implementation of clinical pathways for stroke on a cooperative basis by three hospitals in the same community. The participating institutions developed separate pathways which met their respective organizational needs. This process occurred within separate hospital management structures with coordination among the institutions. They employed a common set of length of stay, quality and resource variables to evaluate the impact of the pathways.

Cerebrovascular Disorders↗
PubMedDate not supplied

Pathways for continence care: an audit to assess how they are used.

This is a follow-up article to three articles that were published between 2000 and 2001 in the British Journal of Nursing about the development of template pathways for continence care (Bayliss et al, 2000a,b, 2001). It reports on what has happened since the development of these templates. One hundred and forty-four healthcare professionals working in the field of continence care were asked to complete a questionnaire about whether the pathways are being used and what changes have been made to them. The audit found nearly half of the respondents are currently using the pathways and find them an effective method of assessing incontinence and providing equitable quality of care for patients. Many respondents have made changes to the pathways, making them easier to use and adapting them to local practice and the availability of local resources. This was what was anticipated, although the authors noted that variance tracking, which should be the driver for change, had not significantly influenced local pathways. Of those healthcare professionals not using pathways, all said they were still interested in using them, which is particularly encouraging as pathways are promoted in 'Guidelines for Continence Care' (Department of Health, 2000). To provide support to these individuals and encourage the efforts of those already using the pathways, a support group is to be established following a further conference on pathways for continence care later this year. It will be the role of this group to facilitate information sharing on pathway development. As a first step in the dissemination of information, a pack is being produced comprising consolidated versions of the changes to the pathways used in practice all over the country.

Clinical Nursing Research↗
PubMedDate not supplied

Care pathways development and implementation.

Care pathways are increasingly being used in the UK as a tool for managing clinical processes and patient outcomes. This article describes some of the key elements of care pathways, highlights factors in successful implementation and discusses some concerns about their use.

Critical Pathways↗
PubMedDate not supplied

Strategic considerations in clinical laboratory management: a laboratory leadership role in clinical pathways. Establishing the laboratory's direct contribution to the institution's performance.

This clinical laboratory serves a unique, though incompletely recognized, function in medical care as the source, moderator, and conduit of vital information supporting the detection, confirmation, and monitoring of disease states. To carry out that function effectively, the laboratory must actively participate in developing clinical pathways based on medical programs. Clinical pathways define the operational and quality requirements for the services involved in meeting the medical program objectives. Because of the laboratory's unique position in the acquisition and flow of information, its contribution must continue as a planned process--based on accurate assessment of value, cost, and resource inputs--rather than in a discrete, event-driven manner. Two examples of clinical pathway development, partly given by the laboratory, illustrate its application in nutritional screening and monitoring for metabolic support and in emergency department admitting decisions on myocardial damage at Bridgeport Hospital (Bridgeport, CT). The paper suggest two activities, point-of-care testing and screening for fetal lung development, that could benefit considerably from clinical pathway information shared across the experiences of several institutions.

Chest Pain↗
PubMed2003

Stroke centers can cut LOS, boost outcomes.

The center is not so much a place as an organized response system. Team meets in-hospital on regular basis to discuss patient progress. Pathway for acute stroke care is an essential ingredient in the formula for success.

Academic Medical Centers↗
PubMed2005

Integrins as linker proteins between osteoblasts and bone replacing materials. A critical review.

The adhesion of osteoblasts to substrates is mediated through proteins that have adsorbed to the substrate, providing integrins on the cell membrane with ligands to connect to. The integrins regulate cell behavior through bi-directional signaling pathways. This critical review has the purpose to consider the research that has been performed with osteoblasts, integrins, and bone replacing materials. Until now, most research has been done to investigate the integrin expression of osteoblasts in culture during cellular adhesion. However, it remains difficult to draw general conclusions from this research. Nevertheless, it can be concluded that the used substrates and protein or peptide coatings can influence the integrin expression and cellular behavior. Additional research has to be done to fully understand all the parameters involved in integrin expression, the adhesion of cells to substrates, and the subsequent cellular behavior. For this purpose, model substrates are under development. The signaling pathway is receiving more and more attention, but for biomaterial purposes, too little consideration is paid to the translation of the in vitro results to the in vivo situation, and to practical applications.

Animals↗
PubMed2007

Disease-associated casein kinase I delta mutation may promote adenomatous polyps formation via a Wnt/beta-catenin independent mechanism.

The Wnt signaling pathway is critical for embryonic development and is dysregulated in multiple cancers. Two closely related isoforms of casein kinase I (CKIdelta and epsilon) are positive regulators of this pathway. We speculated that mutations in the autoinhibitory domain of CKIdelta/epsilon might upregulate CKIdelta/epsilon activity and hence Wnt signaling and increase the risk of adenomatous polyps and colon cancer. Exons encoding the CKIepsilon and CKIdelta regulatory domains were sequenced from DNA obtained from individuals with adenomatous polyps and a family history of colon cancer unaffected by familial adenomatous polyposis or hereditary nonpolyposis colorectal cancer (HNPCC). A CKIdelta missense mutation, changing a highly conserved residue, Arg324, to His (R324H), was found in an individual with large and multiple polyps diagnosed at a relatively young age. Two findings indicate that this mutation is biologically active. First, ectopic ventral expression of CKIdelta(R324H) in Xenopus embryos results in secondary axis formation with an additional distinctive phenotype (altered morphological movements) similar to that seen with unregulated CKIepsilon. Second, CKIdelta(R324H) is more potent than wildtype CKIdelta in transformation of RKO colon cancer cells. Although the R324H mutation does not significantly change CKIdelta kinase activity in an in vitro kinase assay or Wnt/beta-catenin signal transduction as assessed by a beta-catenin reporter assay, it alters morphogenetic movements via a beta-catenin-independent mechanism in early Xenopus development. This novel human CKIdelta mutation may alter the physiological role and enhance the transforming ability of CKIdelta through a Wnt/beta-catenin independent mechanism and thereby influence colonic adenoma development.

Adenomatous Polyps↗
PubMed2006

The 14-3-3 protein FTT-2 regulates DAF-16 in Caenorhabditis elegans.

The Caenorhabditis elegans daf-2/insulin-like signaling pathway is critical for regulating development, longevity, metabolism and stress resistance. We identified the 14-3-3 protein FTT-2 to be a new regulatory component of this pathway. We found that RNAi knock down of ftt-2 specifically enhanced the daf-2-mediated dauer formation phenotype. Furthermore, ftt-2 knock down caused the nuclear accumulation of DAF-16/FOXO, the forkhead transcription factor that is the major downstream effecter of daf-2/insulin-like signaling, and enhanced the transcriptional activities of DAF-16. In contrast to ftt-2, RNAi knock down of par-5/ftt-1, the only other gene predicted to encode a 14-3-3 protein in C. elegans, did not show any notable effect on dauer formation, DAF-16 localization, or DAF-16 downstream gene transcription, underscoring the functional specification of FTT-2 and PAR-5 despite their high sequence homology. Using co-immunoprecipitation, we revealed that FTT-2 formed a complex with GFP-fused DAF-16 in C. elegans. Our results indicate that FTT-2 binds to DAF-16 in C. elegans and regulates DAF-16 by sequestering it in the cytoplasm. A similar mechanism of regulation of FOXO by 14-3-3zeta has been reported in mammalian cells, highlighting the high degree of conservation of the daf-2/insulin-like signaling pathway.

Animals↗
PubMed2005

Cyclin D1 is not an immediate target of beta-catenin following Apc loss in the intestine.

Cyclin D1 is postulated to be a target of the canonical Wnt pathway and critical for intestinal adenoma development. We show here that, unlike cyclin D1 reporter assays, endogenous cyclin D1 levels are not affected following antagonism of the Wnt pathway in vitro, nor is cyclin D1 immediately up-regulated following conditional loss of Apc in vivo. Cyclin D1 levels do, however, increase in a delayed manner in a small subset of cells, suggesting such up-regulation occurs as a secondary event. We also analyzed the immediate consequences of Apc loss in a cyclin D1(-/-) background and failed to find any cyclin D1-dependent phenotypes. However, we did observe elevated cyclin D1 expression in lesions developing 20 days after Apc loss. In these circumstances, all adenomas (but not smaller lesions) showed cyclin D1 up-regulation. Finally in a smaller study, we analyzed whether cyclin D1 deficiency affected adenoma formation 20 days following induced loss of Apc. Unlike AhCre(+) Apc(fl/fl) mice (which all developed adenomas), doubly mutant AhCre(+) Apc(fl/fl) cyclin D1(-/-) mice only developed small lesions. Taken together, this argues that cyclin D1 up-regulation in intestinal neoplasia is important for tumor progression rather than initiation.

Adenoma↗
PubMed2004

Defective insulin secretion and increased susceptibility to experimental diabetes are induced by reduced Akt activity in pancreatic islet beta cells.

The insulin and IGF signaling pathways are critical for development and maintenance of pancreatic beta cell mass and function. The serine-threonine kinase Akt is one of several mediators regulated by these pathways. We have studied the role of Akt in pancreatic beta cell physiology by generating transgenic mice expressing a kinase-dead mutant of this enzyme in beta cells. Reduction of Akt activity in transgenic animals resulted in impaired glucose tolerance due to defective insulin secretion. The mechanisms involved in dysregulation of secretion in these mice lie at the level of insulin exocytosis and are not the result of abnormalities in glucose signaling or function of voltage-gated Ca2+ channels. Therefore, transgenic mice showed increased susceptibility to developing glucose intolerance and diabetes following fat feeding. These observations suggest that Akt plays a novel and important role in the regulation of distal components of the secretory pathway and that this enzyme represents a therapeutic target for improvement of beta cell function in diabetes.

Animals↗
PubMed2003

Map kinase signaling pathways and hematologic malignancies.

Mitogen-activated protein (Map) kinases are widely expressed serine-threonine kinases that mediate important regulatory signals in the cell. Three major groups of Map kinases exist: the p38 Map kinase family, the extracellular signal-regulated kinase (Erk) family, and the c-Jun NH2-terminal kinase (JNK) family. The members of the different Map kinase groups participate in the generation of various cellular responses, including gene transcription, induction of cell death or maintenance of cell survival, malignant transformation, and regulation of cell-cycle progression. Depending on the specific family isoform involved and the cellular context, Map kinase pathways can mediate signals that either promote or suppress the growth of malignant hematopoietic cells. Over the last few years, extensive work by several groups has established that Map kinase pathways play critical roles in the pathogenesis of various hematologic malignancies, providing new molecular targets for future therapeutic approaches. In this review, the involvement of various Map kinase pathways in the pathophysiology of hematologic malignances is summarized and the clinical implications of the recent advances in the field are discussed.

Cytokines↗