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Results for “Critical Pathways”

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At least 1,207 records · Page 67Linked to original sources
PubMed2001

The Rb/E2F pathway and cancer.

Over the past decade, studies focusing on the mechanisms controlling cellular proliferation have converged with equally intensive efforts directed at the analysis of oncogenic pathways associated with human cancer. These convergent studies have revealed the central role played by the pathway that controls the activity of the retinoblastoma tumor suppressor protein (Rb), which in turn regulates the E2F transcription factor. In particular, it is now clear that the Rb/E2F pathway is critical in regulating the initiation of DNA replication. It is also clear that the control of the pathway is disrupted in virtually all human cancers. Questions remain, however, as to the specific role played by individual activities within the pathway in the control of cell growth and their participation in the development of cancer.

Animals↗
PubMed1976

Role of centrifugal pathways to cochlear nucleus in determination of critical bandwidth.

Atropine sulfate was applied locally to the cochlear nucleus of three unanesthetized cats in order to block the cholinergic centrifugal innervation of the nucleus. The critical bandwidth was measured behaviorally from the masked thresholds of 1-kHz tone pips in different bandwidths of masking noise. Atropine increased the critical bandwidth markedly. This suggests that normally the centrifugal pathways influence the critical bandwidth. Saline solutions alone had no effect, and if the cannula was not accurately implanted over the cochlear nucleus, atropine had no effect either.

Acoustic Stimulation↗
PubMed2002

In-hospital care pathways for stroke.

BACKGROUND: Care within a stroke unit reduces death or dependency after stroke. However, studies have found significant variations in clinical practice, access to stroke unit care, organisation of patient care, and clinical outcome. Stroke care pathways have been introduced as a method to promote organised and efficient patient care that is based on best evidence and guidelines. OBJECTIVES: We aimed to assess the effects of care pathways, as compared to standard medical care, among patients with acute stroke who had been admitted to hospital. SEARCH STRATEGY: We searched the Cochrane Stroke Group Specialised Trials Register (last searched in May 2001), the Cochrane Controlled Trials Register (Issue 4, 2000), MEDLINE (1975-2000), EMBASE (1980-2000), CINAHL (1982-2000), the Index to Scientific and Technical Proceedings (ISTP, May 2001), and HealthSTAR (May 2001). We also handsearched the Journal of Managed Care (1997 to 1998), which was later renamed the Journal of Integrated Care (1998 to 2001). Reference lists of articles were searched. SELECTION CRITERIA: We considered randomised controlled trials and non-randomised studies (quasi-randomised trials, comparative studies, controlled and uncontrolled before and after studies, and interrupted time series) that compared care pathway care with standard medical care. DATA COLLECTION AND ANALYSIS: One reviewer selected studies for inclusion and the other independently checked the decisions. Two reviewers independently assessed the methodological quality of the studies. One reviewer extracted the data and the other checked the extracted data. Data from randomised and non-randomised studies were analysed separately. We found significant statistical heterogeneity in the analysis of two outcomes (computed tomography brain scanning and duration of stay). MAIN RESULTS: There were three randomised controlled trials (total of 340 patients) and seven non-randomised studies (total of 1673 patients) that compared care pathway care with standard medical care. We found no difference between care pathway and control groups in terms of death, dependency, or discharge destination. Evidence from mainly non-randomised studies suggests that patients managed using a care pathway may be: a) less likely to suffer a urinary tract infection (OR 0.38, CI 0.18 to 0.79), b) less likely to be readmitted (OR 0.11, CI 0.03 to 0.39), and c) more likely to have a computed tomography brain scan (OR 3.66, CI 1.45 to 9.27) or carotid duplex study (OR 2.45, CI 1.3 to 4.61). Evidence from randomised trials suggests that patient satisfaction and quality of life may be significantly lower in the care pathway group (P=0.02 and P<0.005 respectively). REVIEWER'S CONCLUSIONS: The use of care pathways to manage stroke patients in hospital may be associated with both positive and negative effects on the process of care and clinical outcomes. Since most of the results have been derived from non-randomised studies, they are likely to be influenced by potential biases and confounding factors. There is currently insufficient supporting evidence to justify routine implementation of care pathways for acute stroke management or stroke rehabilitation.

Critical Pathways↗
PubMed2004

In-hospital care pathways for stroke.

BACKGROUND: Stroke care pathways have the potential to promote organised and efficient patient care that is based on best evidence and guidelines, but evidence to support their use is unclear. OBJECTIVES: We aimed to assess the effects of care pathways, compared with standard medical care, among patients with acute stroke who had been admitted to hospital. SEARCH STRATEGY: We searched the Cochrane Stroke Group Trials Register (last searched in June 2003), the Cochrane Central Register of Controlled Trials (The Cochrane Library, Issue 2, 2003), MEDLINE (1975 to June 2003), EMBASE (1980 to June 2003), CINAHL (1982 to June 2003), ISI Proceedings: Science & Technology (1990 to November 2003), and HealthSTAR (1994 to May 2001). We also handsearched the Journal of Integrated Care Pathways (2001 to 2003), formerly Journal of Managed Care (1997 to 1998) and Journal of Integrated Care (1998 to 2001). Reference lists of articles were searched. SELECTION CRITERIA: We considered randomised controlled trials and non-randomised studies that compared care pathway care with standard medical care. DATA COLLECTION AND ANALYSIS: One reviewer selected studies for inclusion and the other independently checked the decisions. Two reviewers independently assessed the methodological quality of the studies. One reviewer extracted the data and the other checked the extracted data. MAIN RESULTS: Three randomised controlled trials (340 patients) and 12 non-randomised studies (4081 patients) were included. There was significant statistical heterogeneity in the analysis of many of the outcomes. We found no significant difference between care pathway and control groups in terms of death or discharge destination. Patients managed with a care pathway were: (a) more dependent at discharge (P = 0.04); (b) less likely to suffer a urinary tract infection (Odds Ratio (OR) 0.51, 95% Confidence Interval (CI) 0.34 to 0.79); (c) less likely to be readmitted (OR 0.11, 95% CI 0.03 to 0.39); and (d) more likely to have neuroimaging (OR 2.42, 95% CI 1.12 to 5.25). Evidence from randomised trials suggested that patient satisfaction and quality of life were significantly lower in the care pathway group (P = 0.02 and P < 0.005 respectively). REVIEWERS' CONCLUSIONS: Use of stroke care pathways may be associated with positive and negative effects. Since most of the results have been derived from non-randomised studies, they are likely to be influenced by potential biases and confounding factors. There is currently insufficient supporting evidence to justify the routine implementation of care pathways for acute stroke management or stroke rehabilitation.

Critical Pathways↗
PubMed2003

Calcineurin-mediated pathway involved in the differentiated phenotype of smooth muscle cells.

The calcineurin-mediated pathway is involved in skeletal and cardiac hypertrophy and vascular development in vivo, but the relationship between this pathway and the phenotype of smooth muscle cells (SMCs) remains unknown. Using visceral SMCs in culture as a model system of differentiated SMCs, we investigated the role of the calcineurin-mediated pathway in maintaining the differentiated phenotype of SMCs, which depends on the insulin-like growth factor (IGF-I)-triggered activation of the phosphatidylinositol 3-kinase (PI3-K)/protein kinase B (PKB(Akt)) pathway. Treatment with calcineurin inhibitors, cyclosporin A or FK506, or the forced expression of the natural calcineurin inhibitor, CAIN, induced SMC dedifferentiation. Notably, suppression of the promoter activities of the SMC molecular markers caldesmon and alpha1 integrin by blocking the PI3-K/PKB(Akt) pathway was rescued by the forced expression of constitutively active calcineurin Aalpha, suggesting that the calcineurin-mediated pathway is critical for maintaining the differentiated phenotype of SMCs and works downstream of the PI3-K/PKB(Akt) pathway.

Animals↗
PubMed1994

Regulation of ATP-ubiquitin-dependent proteolysis in muscle wasting.

Protein breakdown plays a major role in muscle growth and atrophy. However, the regulation of muscle proteolysis by nutritional, hormonal and mechanical factors remains poorly understood. In this review, the methods available to study skeletal muscle protein breakdown, and our current understanding of the role of 3 major proteolytic systems that are well characterized in this tissue (ie the lysosomal, Ca(2+)-dependent and ATP-ubiquitin-dependent proteolytic pathways) are critically analyzed. ATP-ubiquitin-dependent proteolysis is discussed in particular since recent data strongly suggest that this pathway may be responsible for the loss of myofibrillar proteins in many muscle-wasting conditions in rodents. In striking contrast to either the lysosomal or the Ca(2+)-dependent processes, ATP-ubiquitin-dependent protein breakdown is systematically influenced by nutritional manipulation (fasting and dietary protein deficiency), muscle activity and disuse (denervation atrophy and simulated weightlessness), as well as pathological conditions (sepsis, cancer, trauma and acidosis). The hormonal control of this pathway, its possible substrates, rate-limiting step, and functional associations with other proteolytic systems are discussed.

Adenosine Triphosphate↗
PubMed2006

Handicapping the race to develop inhibitors of the phosphoinositide 3-kinase/Akt/mammalian target of rapamycin pathway.

The phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway controls many cellular processes that are important for the formation and progression of cancer, including apoptosis, transcription, translation, metabolism, angiogenesis, and cell cycle progression. Genetic alterations and biochemical activation of the pathway are frequent events in preneoplastic lesions and advanced cancers and often portend a poor prognosis. Thus, inhibition of the PI3K/Akt/mTOR pathway is an attractive concept for cancer prevention and/or therapy. Inhibitors of individual components, such as PI3K, PDK-1, Akt, and mTOR, are being developed at a rapid pace and have promise for improving the care of cancer patients. Here, we review the published data on inhibitors of the pathway and discuss relevant issues, such as the complex regulation of the pathway, the design of clinical trials, and the likelihood of finding a therapeutic index when targeting such a critical signaling pathway.

3-Phosphoinositide-Dependent Protein Kinases↗