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PubMedDate not supplied

The impact of a burn wound education program and implementation of a clinical pathway on patient outcomes.

Patients are often discharged before burn wounds are fully healed, which requires home care nurses to manage complex burn care. This study evaluated patient outcomes at 3 periods: (1) before visiting nurses participated in a burn care education program, (2) after visiting nurses participated in a burn education program, and (3) after the implementation of a burn clinical pathway. A random sample of 54 patient records from the first 2 periods and the entire sample of 12 records from the third period were reviewed. Demographic variables included age, sex, race, percentage of total body surface area burned, and mechanism of burn. Outcome variables measured were weight maintenance, wound infection, pain management, unplanned readmissions to the burn unit, and documentation of patient education. The findings of this study show the positive impact of education in combination with the use of a burn home care clinical pathway.

Adolescent↗

PubMedDate not supplied

Nurse case managers: patient care implications at a Pakistani university.

The role of the nurse in hospital is varied and some are choosing to incorporate more managerial and administrative skills into their clinical role. One such role is that of the nurse case manager (NCM). This particular role concentrates on involving the family and the patient in his or her own care, facilitation of the care plan, and open discussions between the patient, medics and nursing staff. NCMs in the author's hospital have made a remarkable contribution to patient care. It is a challenging and exceedingly demanding role in both developing and developed countries, but one that is increasingly important. The NCMs are involved in coordination, facilitation of core process and mobilization of resources, not only in hospital but at the patient's home. In this short introductory article the role of NCM is highlighted and the author discusses how this diverse role is concerned with patient care. NCMs work with multidisciplinary teams to enhance the patient's care process. Their attention is also given to cost reduction and clinical pathway management.

Case Management↗

PubMed1997

COPD pathway cuts costs per case by $900.

Mobile (AL) Infirmary Medical Center's clinical pathway for chronic obstructive pulmonary disease (COPD) has cut length of stay from 7.8 days to 5.6 days, and cut costs per case from $4,050 to $3,170, resulting in an annual profit of more than $300,000. One reason for the pathway's high degree of physician buy-in has been case managers' willingness to make changes to the pathway with a minimum of red tape. One early revision to the COPD pathway was the development of specific patient goals for each day of the path. Other revisions included making the pathway a permanent part of the medical record and attaching relevant protocols to the pathway, such as a protocol for oxygen therapy.

Alabama↗

PubMed2006

[Clinical pathways in the treatment of cancers].

At the beginning, a clinical pathway was first introduced for the purpose of standardizing the treatment, providing high quality management and shortening hospital stays in the managed care health system in USA. This has been rapidly accepted also in Japan. The clinical pathway has also been gradually introduced in the treatment of malignant diseases, including chemo/radiotherapy and surgery. In Kurume University Hospital, clinical pathways are now applied for 50% of inpatients, and those for cancer patients have a large role in routine clinical practice. The progress of our pathways for cancer patients is here reported.

Critical Pathways↗

PubMed2005

CD70 signaling is critical for CD28-independent CD8+ T cell-mediated alloimmune responses in vivo.

The inability to reproducibly induce robust and durable transplant tolerance using CD28-B7 pathway blockade is in part related to the persistence of alloreactive effector/memory CD8(+) T cells that are less dependent on this pathway for their cellular activation. We studied the role of the novel T cell costimulatory pathway, CD27-CD70, in alloimmunity in the presence and absence of CD28-B7 signaling. CD70 blockade prolonged survival of fully mismatched vascularized cardiac allografts in wild-type murine recipients, and in CD28-deficient mice induced long-term survival while significantly preventing the development of chronic allograft vasculopathy. CD70 blockade had little effect on CD4(+) T cell function but prevented CD8(+) T cell-mediated rejection, inhibited the proliferation and activation of effector CD8(+) T cells, and diminished the expansion of effector and memory CD8(+) T cells in vivo. Thus, the CD27-CD70 pathway is critical for CD28-independent effector/memory CD8(+) alloreactive T cell activation in vivo. These novel findings have important implications for the development of transplantation tolerance-inducing strategies in primates and humans, in which CD8(+) T cell depletion is currently mandatory.

Acute Disease↗

PubMed2002

Hypercoagulability test strategies in the protein C and protein S pathway.

The protein C-protein S pathway is critical in controlling normal clot formation to provide homeostasis between thrombosis and hemorrhage. Abnormalities have been described in which the pathway is altered because factor V cannot be degraded by activated protein C, producing activated protein C resistance. It has been known for nearly two decades that deficiencies in protein C and protein S can result in impaired inhibition of clot formation resulting in increased risk for thrombosis. This article describes the testing strategies associated with the diagnosis of activated protein C resistance, protein C deficiency, and protein S deficiency.

Algorithms↗

PubMed2006

Antitumorigenic effect of Wnt 7a and Fzd 9 in non-small cell lung cancer cells is mediated through ERK-5-dependent activation of peroxisome proliferator-activated receptor gamma.

The Wnt pathway is critical for normal development, and mutation of specific components is seen in carcinomas of diverse origins. The role of this pathway in lung tumorigenesis has not been clearly established. Recent studies from our laboratory indicate that combined expression of the combination of Wnt 7a and Frizzled 9 (Fzd 9) in Non-small Cell Lung Cancer (NSCLC) cell lines inhibits transformed growth. We have also shown that increased expression of peroxisome proliferator-activated receptor gamma (PPARgamma) inhibits transformed growth of NSCLC and promotes epithelial differentiation of these cells. The goal of this study was to determine whether the effects of Wnt 7a/Fzd 9 were mediated through PPARgamma. We found that Wnt 7a and Fzd 9 expression led to increased PPARgamma activity. This effect was not mediated by altered expression of the protein. Wnt 7a and Fzd 9 expression resulted in activation of ERK5, which was required for PPARgamma activation in NSCLC. SR 202, a known PPARgamma inhibitor, blocked the increase in PPARgamma activity and restored anchorage-independent growth in NSCLC expressing Wnt 7a and Fzd 9. SR 202 also reversed the increase in E-cadherin expression mediated by Wnt 7a and Fzd 9. These data suggest that ERK5-dependent activation of PPARgamma represents a major effector pathway mediating the anti-tumorigenic effects of Wnt 7a and Fzd 9 in NSCLC.

Antineoplastic Agents↗

PubMed2005

Atherosclerosis and innate immune signaling.

Atherosclerosis, the leading cause of death in developed countries, is characterized by chronic inflammation in the artery wall. It has been appreciated for decades that this disease is linked to hypercholesterolemia and the accumulation of macrophages in the artery wall, yet the exact mechanisms underlying this inflammatory process remain unclear. The role of innate and adaptive immune responses in the pathogenesis of atherosclerosis has been an area of intense study. It now appears that activation of innate immune signaling pathways designed to protect us from microbes may be responsible for initiating and feeding the chronic inflammatory cascade that characterizes this disease. In this review, we discuss the recent identification of Toll-like receptors and their downstream signaling pathways as critical contributors to atherosclerosis. Unraveling the contribution of individual Toll-like receptors and identifying the ligands that activate these pathways will be a central focus of atherosclerosis research in the next few years. The involvement of these pathways in atherogenesis will not only open up new avenues of investigation, but it also provides new targets for therapeutic manipulation that could ameliorate the atherosclerotic inflammatory response directly.

Arteriosclerosis↗

PubMed2003

MEK inhibition of pancreatic carcinoma cells by U0126 and its effect in combination with sulindac.

OBJECTIVES: The MAP kinase kinase (MEK)-extracellular signal-regulated kinase (ERK) pathway is critical for cell growth and survival. In the current study, we examined the effect of inhibiting the MEK-ERK pathway in pancreatic tumor cells with the MEK-specific inhibitor U0126. In addition, we investigated whether the MEK-ERK pathway influenced the response of pancreatic cancer cells to nonsteroidal antiinflammatory drugs (NSAIDs). METHODS: Cell growth was monitored by a colorimetric proliferation assay and cell counts. Cell cycle analysis was performed using flow cytometry. Apoptosis was measured using a DNA fragmentation ELISA. Protein expression was detected by Western blot. CONCLUSION: Treatment with U0126 dose dependently inhibited the growth of 3 human pancreatic carcinoma cell lines (BxPC-3, PANC-1, and MIA PaCa-2). U0126 treatment resulted in cell-cycle alterations but did not induce apoptosis. Growth inhibitory concentrations of NSAIDs unexpectedly increased ERK phosphorylation in BxPC-3 and MIA PaCa-2 cells. We therefore evaluated the effect of treating pancreatic tumor cells with the combination of the NSAID sulindac and U0126. Treatment with U0126 complemented sulindac-induced growth inhibition in BxPC-3 and PANC-1 cells. The expression of several cell cycle (p21, p27, cyclin D1) and apoptotic (survivin, Bcl-xL) regulatory proteins was altered after U0126 and/or sulindac treatment. Our findings suggest that inhibition of the MEK-ERK signaling pathway may sensitize pancreatic tumor cells to NSAID therapy.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2006

Site-specific casein kinase 1epsilon-dependent phosphorylation of Dishevelled modulates beta-catenin signaling.

Careful regulation of the Wnt-Beta-catenin signaling pathway is critical to many aspects of development and cancer. Casein kinase Iepsilon is a Wnt-activated positive regulator of this pathway. Members of the Dishevelled family have been identified as key substrates of casein kinase I (CKI). However, the specific sites phosphorylated in vivo by CKI and their relative importance in the physiologic regulation of these proteins in the canonical Wnt-beta-catenin signaling pathway remain unclear. To address this question, recombinant mouse Dishevelled (mDvl-1) was phosphorylated by CKIin vitro and phosphorylation sites were identified by MS. CKI phosphorylation of mDvl-1 at two highly conserved residues, serines 139 and 142, was observed by MS and confirmed by phosphopeptide mapping of in vivo phosphorylated protein. Phosphorylation of these sites is dependent on casein kinase I epsilon activity in vivo. Phenotypic analysis of mutant mDvl-1 indicates that phosphorylation of these sites stimulates the Dvl-activated beta-catenin-dependent Wnt signaling pathway in both cell culture and in Xenopus development. Casein kinase I epsilon is a Wnt-regulated kinase, and regulated phosphorylation of Dvl allows fine tuning of the Wnt-beta-catenin signaling pathway.

Adaptor Proteins, Signal Transducing↗

PubMed2006

Jasmonate signaling pathway.

Jasmonates in plants are cyclic fatty acid-derived regulators structurally similar to prostaglandins in metazoans. These chemicals mediate many of plants' transcriptional responses to wounding and pathogenesis by acting as potent regulators for the expression of numerous frontline immune response genes, including those for defensins and antifungal proteins. Additionally, the pathway is critical for fertility. Ongoing genetic screens and protein-protein interaction assays are identifying components of the canonical jasmonate signaling pathway. A massive molecular machine, based on two multiprotein complexes, SCF(COI1) and the COP9 signalosome (CNS), plays a central role in jasmonate signaling. This machine functions in vivo as a ubiquitin ligase complex, probably targeting regulatory proteins, some of which are expected to be transcriptional repressors. Some defense-related mediators, notably salicylic acid, antagonize jasmonates in controlling the expression of many genes. In Arabidopsis, NONEXPRESSOR OF PR GENES (NPR1) mediates part of this interaction, with another layer of control provided further downstream by the mitogen-activated protein kinase (MAPK) homolog MPK4. Numerous other interpathway connections influence the jasmonate pathway. Insights from Arabidopsis have shown that an allele of the auxin signaling gene AXR1, for example, reduces the sensitivity of plants to jasmonate. APETALA2 (AP2)-domain transcription factors, such as ETHYLENE RESPONSE FACTOR 1 (ERF1), link the jasmonate pathway to the ethylene signaling pathway. As progress in characterizing several new mutants (some of which are hypersensitive to jasmonic acid) augments our understanding of jasmonate signaling, the Connections Map will be updated to include this new information.

Arabidopsis↗

PubMed2006

Identification of genes regulated by Wnt/beta-catenin pathway and involved in apoptosis via microarray analysis.

BACKGROUND: Wnt/beta-catenin pathway has critical roles in development and oncogenesis. Although significant progress has been made in understanding the downstream signaling cascade of this pathway, little is known regarding Wnt/beta-catenin pathway modification of the cellular apoptosis. METHODS: To identify potential genes regulated by Wnt/beta-catenin pathway and involved in apoptosis, we used a stably integrated, inducible RNA interference (RNAi) vector to specific inhibit the expression and the transcriptional activity of beta-catenin in HeLa cells. Meanwhile, we designed an oligonucleotide microarray covering 1384 apoptosis-related genes. Using oligonucleotide microarrays, a series of differential expression of genes was identified and further confirmed by RT-PCR. RESULTS: Stably integrated inducible RNAi vector could effectively suppress beta-catenin expression and the transcriptional activity of beta-catenin/TCF. Meanwhile, depletion of beta-catenin in this manner made the cells more sensitive to apoptosis. 130 genes involved in some important cell-apoptotic pathways, such as PTEN-PI3K-AKT pathway, NF-kappaB pathway and p53 pathway, showed significant alteration in their expression level after the knockdown of beta-catenin. CONCLUSION: Coupling RNAi knockdown with microarray and RT-PCR analyses proves to be a versatile strategy for identifying genes regulated by Wnt/beta-catenin pathway and for a better understanding the role of this pathway in apoptosis. Some of the identified beta-catenin/TCF directed or indirected target genes may represent excellent targets to limit tumor growth.

Apoptosis↗

PubMedDate not supplied