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Biomedical subjects

P L Chang

Publications and source records attributed to P L Chang.

At least 19 recordsLinked to original sources
PubMed2002

Improvement of practice performance in urological surgery via clinical pathway implementation.

The purpose of this study was to compare performance measurements to evaluate the effects of clinical pathway implementation on improving practice performances in urology. Since April 1997, a total of 18 clinical pathways have been created in the urology department. Of these clinical pathways, six were implemented for endoscopic surgery, and four and eight were for minor and major surgery, respectively. Eight prominent performance measurements, which were identified as representative indicators of the practice performances, were selected in endoscopic surgery, five in minor surgery, and 11 in major surgery. Between April 1997 and March 1999, 2,883 consecutive patients, who underwent endoscopic surgery, minor surgery, and major surgery, were evaluated herein. The treatment results for patients in the first and second years of clinical pathway implementation were compared to those from the year preceding the implementation. In endoscopic surgery, five of the eight performance measurements improved significantly in the first year of implementation. Notably, three of the five improved performances continued to improve in the second year. Similarly, in minor surgery, four of the five performance measurements improved significantly following 2 years. Finally, in major urological surgery, six of the 11 performance measurements also improved significantly after 1 year; four of which continued to improve during the second year. Therefore, we conclude that patient care, which is based on the implementation of clinical pathways, can improve practice performances and facilitate medical care.

Critical Pathways↗
PubMed2002

The differences in health outcomes between Web-based and paper-based implementation of a clinical pathway for radical nephrectomy.

OBJECTIVE: To evaluate the effects of a web-based clinical pathway (WCP) for radical nephrectomy on patient care, and to compare the effects with those of a paper-based clinical pathway (PCP). PATIENTS AND METHODS: Patients with renal cell carcinoma and who underwent radical nephrectomy were enrolled into the study. The results of using the WCP for radical nephrectomy from July 2000 to August 2001 were compared with those using the PCP between May 1999 and June 2000. The mean hospital stay, average admission charges, six quality indicators, and the advantages of the WCP were determined. RESULTS: Using a WCP for radical nephrectomy reduced the hospital stay and admission charges by as much as the PCP. A similar number of patients had variances from the WCP as with the PCP (P = 0.407), but the number of undetected variances and the variance detection time in the WCP were significantly less (P = 0.0193 and 0.0162). Implementing a WCP also improved the quality of care by as much as a PCP. CONCLUSIONS: Using a WCP for radical nephrectomy can improve health outcomes by reducing the hospital stay and admission charges, and by improving the quality of care by as much as a PCP. Furthermore, the WCP was more accurate and faster than the PCP in detecting variances.

Adult↗
PubMed2002

Treatment of hemophilia B in mice with nonautologous somatic gene therapeutics.

The implantation of nonautologous cells encapsulated in immunoprotective microcapsules provides an alternative nonviral method for gene therapy. This strategy was successful in reversing the disease phenotypes of dwarfism and a lysosomal storage disease, mucopolysaccharidosis VII, in murine models. In this article we implanted transgenic hemophilic B mice with microcapsules enclosing factor IX-secreting C2C12 myoblasts to study the clinical potential of this approach in the treatment of hemophilia. Treated mice showed increased plasma factor IX levels as high as 28 ng of human factor IX per milliliter of plasma and decreased activated thromboplastin times (reduced by 20% to 29%). However, the level of factor IX decreased to baseline levels by day 7, coinciding with emergence of anti-human factor IX antibody, the titer of which increased greater than 10-fold by day 28. Monoclonal anti-CD4 antibodies were used to deplete CD4+ T cells to suppress the immune response against the recombinant factor IX. In the treated hemophilic mice, the anti-factor IX antibody response was totally suppressed to beyond day 28 accompanied by a significant decrease in activated thromboplastin time compared with that seen in untreated hemophilic mice. When the microcapsules were recovered from the intraperitoneal cavity after 38 days of implantation, the encapsulated cells continued to secrete factor IX at preimplantation levels, but both cell viability and microcapsule mechanical stability were reduced. Hence although the polymer chemistry of the microcapsules and cell viability may need to be improved for long-term delivery, nonautologous gene therapy with microencapsulated cells has been shown to be effective, at least for the short-term, in alleviating the hemophilic hemostatic anomaly. Coadministration of an immunosuppressant is effective in inhibiting antibody development against the delivered factor IX and should be considered for recipients at risk of inhibitor development.

Animals↗
PubMed2002

Deterioration of polyamino acid-coated alginate microcapsules in vivo.

The implantation of immuno-isolated recombinant cell lines secreting a therapeutic protein in alginate microcapsules presents an alternative approach to gene therapy. Its clinical efficacy has recently been demonstrated in treating several genetic diseases in murine models. However, its application to humans will depend on the long-term structural stability of the microcapsules. Based on previous implantations in canines, it appears that survival of alginate-poly-L-lysine-alginate microcapsules in such large animals is short-lived. This article reports on the biological factors that may have contributed to the degradation of these microcapsules after implantation in dogs. Alginate microcapsules coated with poly-L-lysine or poly-L-arginine were implanted in subcutaneous or intraperitoneal sites. The retrieved microcapsules showed a loss of mechanical stability, as measured by resistance to osmotic stress. The polyamino acid coats were rendered fragile and easily lost, particularly when poly-L-lysine was used for coating and the intraperitoneal site was used for implantation. Various plasma proteins were associated with the retrieved microcapsules and identified with western blotting to include Factor XI, Factor XII, prekallikrein, HMWK, fibrinogen, plasminogen, ATIII, transferrin, alpha-1-antitrypsin, fibronectin, IgG, alpha-2-macroglobulin, vitronectin, prothrombin, apolipoprotein A1, and particularly albumin, a major Ca-transporting plasma protein. Complement proteins (C3, Factor B, Factor H, Factor I) and C3 activation fragments were detected. Release of the amino acids from the microcapsule polyamino acid coats was observed after incubation with plasma. indicating the occurrence of proteolytic degradation. Hence, the loss of long-term stability of the polyamino acid-coated alginate microcapsules is associated with activation of the complement system, degradation of the polyamino acid coating, and destabilization of the alginate core matrix, probably through loss of calcium-mediated ionic cross-linking of the guluronic acid polymers in the alginate. These destructive forces may be slightly mitigated by using poly-L-arginine instead of poly-L-lysine for coating and by implanting in a subcutaneous instead of an intraperitoneal site. However, the long-term stability of such devices may require significant improvements in the microcapsule polymer chemistry to withstand such biological impediments.

Alginates↗
PubMed2002

Development of small alginate microcapsules for recombinant gene product delivery to the rodent brain.

A novel form of gene therapy using encapsulated recombinant cells in alginate microcapsules has proven effective in treating several animal models of human diseases. For treating neurological deficits in rodents with this technology, the size of the microcapsules has to be reduced for implantation in the central nervous system (CNS) to bypass the blood-brain barrier. This article reports the development of small alginate microcapsules suitable for implantation into the mouse CNS. By varying the encapsulation protocol, recombinant cells could be encapsulated in microcapsules ranging in diameter from 5 to 2000 microm. The optimal size for implantation was determined to be 100-200 microm, based on the smallest, homogeneously sized, cell-filled microcapsules that could pass the 500 microm inner diameter of a CNS-implantation needle. Compared with medium-sized (500-700 microm) microcapsules, these small microcapsules packed more tightly together with less inter-capsule space, resulting in an increased number of cells and a higher rate of recombinant gene product secretion per volume of microcapsules. The small microcapsules also displayed increased mechanical strength, compared with large microcapsules. These excellent in vitro properties of small 100-200 microm microcapsules warrant further in vivo investigation into the feasibility of using immuno-isolation gene therapy to deliver recombinant gene products to the rodent CNS.

Alginates↗
PubMed2001

Analysis of large-volume DNA markers and polymerase chain reaction products by capillary electrophoresis in the presence of electroosmotic flow.

We have demonstrated on-line concentration and separation of DNA in the presence of electroosmotic flow (EOF) using poly(ethylene oxide) (PEO) solutions. After injecting large-volumes DNA samples, PEO solutions entered a capillary filled with 400 mM Tris-borate (TB) buffers by EOF and acted as sieving matrices. DNA fragments stacked between the sample zone and PEO solutions. Because sample matrixes affected PEO adsorption on the capillary wall, leading to changes in EOF, migration time, concentration, and resolving power varied with the injection length. When injecting phiX174 RF DNA-HaeIII digest prepared in 5 mM Tris-HCl buffer, pH 7.0, at 250 V/cm, peak height increased linearly as a function of injection volume up to 0.9 microl (injection time 150 s). The sensitivity improvement was 100-fold compare to that injected at 25 V/cm for 10 s (0.006 microl). When injecting 1.54 microl of GeneScan 1000 ROX, the sensitivity improvement was 265-fold. The sensitivity improvement was 40-fold when injecting 0.17 microl DNA sample containing pBR 322/HaeIII, pBR 328/BglI, and pBR 328/HinfI digests prepared in phosphate-buffered saline. This method allows the analysis of polymerase chain reaction (PCR) products amplified after 17 cycles when injecting 0.32 microl (at 30 cm height for 300 s). The total analysis time was shorter (91.6 min) than that (119.6 min) obtained from injecting PCR products after 32 cycles for 10 s.

Base Sequence↗
PubMed2001

Osmotic pressure test: a simple, quantitative method to assess the mechanical stability of alginate microcapsules.

Implantation of microencapsulated, nonautologous cells and tissues is an effective method to deliver therapeutic proteins in vivo. Its success depends on the maintenance of the immunoisolating barrier provided by the microcapsule. Thus, one goal in the development of this technology is to create mechanically stable microcapsules. We have developed an osmotic pressure test to quantify the strength of microcapsules by exposing alginate microcapsules to a graded series of hypotonic solutions and quantifying the percentage of broken microcapsules. The test was validated by confirming the relative strengths of different types of alginate capsules, previously known from implantation in dogs to have differing mechanical stability in vivo. Thus, solid alginate microcapsules crosslinked with Ba(2+) were shown to be stronger than those crosslinked with Ca(2+), which in turn were shown to be stronger than the corresponding hollow alginate microcapsules. The incorporation of cells was demonstrated to reduce the mechanical stability of the microcapsules significantly. Hence, this test provides a simple and quantitative method for rapidly determining the strength of a large number of microcapsules. Thus, it is suitable for monitoring the mechanical stability of various types of microcapsules, predicting the performance of microcapsules in vivo, and for quality control of microcapsules during scale-up productions.

Alginates↗
PubMed2001

Hydroxylapatite binds more serum proteins, purified integrins, and osteoblast precursor cells than titanium or steel.

The implant material hydroxylapatite (HA) has been shown in numerous studies to be highly biocompatible and to osseointegrate well with existing bone; however, the molecular mechanisms at work behind this osseointegration remain largely unexplored. One possibility is that the implant, exposed to the patient's blood during surgery, adsorbs known cell adhesive proteins such as fibronectin and vitronectin from the serum. Osteoblast precursors could then adhere to these proteins through integrin-mediated mechanisms. In the present study, we have used a quantitative ELISA assay to test the hypothesis that hydroxylapatite will adsorb more fibronectin and vitronectin from serum than two commonly used hard-tissue materials, commercially pure titanium, and 316L stainless steel. We further used the ELISA, as well as a standard cell adhesion assay, to test the hypothesis that increased protein adsorption will lead to better binding of purified integrins alpha5beta1 and alpha(v)beta3 and osteoblast precursor cells to the HA than to the metals. Our results show that fibronectin, vitronectin, alpha5beta1, alpha(v)beta3, and osteoblast precursor cells do indeed bind better to HA than to the metals, suggesting that improved integrin-mediated cell binding may be one of the mechanisms leading to better clinical bone integration with HA-coated implants.

Adsorption↗
PubMed2001

Glutamine utilization in activated lymphocytes from rats receiving endotoxin.

BACKGROUND: A beneficial effect of supplemental glutamine for lymphocyte function in patients under metabolic stress has been suggested. Nevertheless, it is not clear how glutamine is used by lymphocytes when under stress. This time course study investigated the effect of endotoxin-induced stress on in vitro glutamine utilization and glutamine-dependent proliferation of activated lymphocytes. METHODS: Metabolic stress was modeled by intraperitoneal (ip) administration of endotoxin (5 mg/kg body wt) to rats. Control animals were injected with sterile saline. Cervical lymph node lymphocytes collected from animals 6, 12, 24, and 48 h following injection were activated with concanavalin A. Proliferation of these activated lymphocytes in the presence of 0.1-2 mM glutamine was determined. The glutamine utilization rate and glutaminase activity in the activated lymphocytes were also determined. RESULTS: The proliferation rate of lymphocytes was not affected by ip administration of endotoxin 6 h following the insult, however, 12, 24, and 48 h following the insult, the maximal response was suppressed (P < 0.05). In addition, at 12, 24, and 48 h, the concentration of glutamine for the maximal response of lymphocytes was lower than that for the control group (P < 0.05). Throughout the investigation period, both the glutamine utilization rate and glutaminase activity in the activated lymphocytes were decreased time-dependently. CONCLUSION: The present study demonstrates that glutamine utilization by lymphocytes under a mitogenic challenge in vitro is significantly decreased in the late period after endotoxin injection. This is at least partly due to decreased glutaminase activity and is associated with decreased proliferation rate of mitogen-activated lymphocytes.

Animals↗
PubMed2001

Posthumous reproduction in a human immunodeficiency virus-discordant couple.

A human immunodeficiency virus-discordant couple failed to conceive through in vitro fertilization and intracytoplasmic sperm injection of cryopreserved semen banked by the human immunodeficiency virus-positive partner. The husband subsequently had acquired immunodeficiency syndrome and died. The subsequent transfer of cryopreserved embryos resulted in pregnancy. Both mother and child are human immunodeficiency virus negative.

Acquired Immunodeficiency Syndrome↗
PubMed2001

Immuno-isolation in oncology--a mini-review.

Immuno-isolation provides a potentially safe and effective method of delivering recombinant therapeutic molecules. Its application as a drug-delivery platform for the treatment of cancer has shown promising developments recently. This review will summarize the principle and current progress of this novel therapy paradigm in oncology. In this approach, a non-autologous cell line is genetically modified to secrete a recombinant product with potential for tumor suppression. Such a cell line may be implanted without graft rejection into all patients with similar neoplastic disease. The immune protection is conferred by enclosure within immuno-isolating devices such as microcapsules whose permeability would allow passage of smaller molecules such as oxygen, nutrients and waste products as well as the desired therapeutic transgene product. However, large immune mediators such as complement, macrophages and lymphocytes responsible for graft rejection would be excluded. In this review, we will consider how this technology may be applied as a novel genetic tool for cancer treatment to deliver antibodies, cytokines, enzymes and growth factors for treatment of various types of cancer. These molecules can be delivered at low constitutive levels, thereby permitting long-term systemic delivery, maintaining biological activity over extended periods, and eliminating the costs of product purification. The current success of this strategy in cancer treatment will be reviewed in in vitro systems, in animal models of cancer, and in human clinical trials.

Animals↗
PubMed2000

Treatment of a lysosomal storage disease, mucopolysaccharidosis VII, with microencapsulated recombinant cells.

Most lysosomal enzyme deficiencies are catastrophic illnesses with no generally available treatments. We have used the beta-glucuronidase-deficient mouse model of mucopolysaccharidosis type VII (MPS VII) to develop an alternative approach to therapy. A "universal" cell line engineered to secrete the missing enzyme is implanted in all recipients requiring the same enzyme replacement. The cells, although nonautologous, are rendered immunologically tolerant by encapsulation in microcapsules that provide protection from immune mediators. Using this strategy, we injected beta-glucuronidase-secreting fibroblasts enclosed in alginate microcapsules into mutant MPS VII mice. After 24 hr, beta-glucuronidase activity was detected in the plasma, reaching 66% of physiological levels by 2 weeks postimplantation. Significant beta-glucuronidase activity was detected in liver and spleen for the duration of the 8-week experiment. Concomitantly, the intralysosomal accumulation of undegraded glycosaminoglycans was dramatically reduced in liver and spleen tissue sections and urinary glycosaminoglycan content was reduced to normal levels. Elevated secondary lysosomal enzymes beta-hexosaminidase and alpha-galactosidase were also reduced. However, implanted mutant MPS VII mice developed antibodies against the murine beta-glucuronidase, demonstrating a potential obstacle in patients with a null mutation who react against the replaced enzyme as a foreign antigen. The antibody response was transiently circumvented with a single treatment of purified anti-CD4 antibody coadministered with the microcapsules. This resulted in increased levels and duration of beta-glucuronidase delivery. Similarly, treated heterozygous mice maintained elevated levels of beta-glucuronidase and did not develop antibodies. This novel cell-based therapy demonstrates a potentially cost-effective and nonviral treatment applicable to all lysosomal storage diseases.

Alleles↗
PubMed2000

Galactosyl receptor, a cell surface C-type lectin of normal and tumoral prostate epithelial cells with binding affinity to endothelial cells.

BACKGROUND: The mechanism of bone metastasis of prostate cancer involves the interaction of cell surface receptor(s) on cancer cells with ligand(s) on bone marrow endothelial cell surfaces. The rat galactosyl receptor gene generates two mRNA species by differential splicing: one species encodes a protein identical to the minor form of hepatocyte asialoglycoprotein receptor and displays a galactose/N-acetyl-galactosamine-recognition domain; the other encodes a protein with identical intracellular and transmembrane domains but with a different extracellular domain lacking the carbohydrate-recognition domain (CRD). Both proteins appear to coexist as a heterooligomer on the surface of normal mouse, rat, and human prostate epithelial cells and human prostate cancer cells, including the PC-3 cell line. The CRD of galactosyl receptor mediates adhesion of normal and tumoral prostate cells to the surfaces of a human bone marrow endothelial cell line. The use of inhibitors targeting the CRD would be very valuable in hindering the binding of prostate cancer cells to endothelial cells, thus decreasing the incidence of hematogenous metastasis to bone. METHODS: Molecular biology, immunohistochemistry, flow cytometry, and a cell aggregation assay were used to determine the expression and role of the galactosyl receptor in cell adhesion. RESULTS: Immunoblotting experiments demonstrated that each component of the heterooligomer has a mass of 54 kDa, ascribed in part to associated carbohydrates. An oligonucleotide probe showed the presence of both galactosyl receptor forms in rat prostate and testis, but not in liver, kidney, and spleen. Antibodies to the CRD and a segment of the nonhomologous extracellular domain of the galactosyl receptor blocked cell adhesion to endothelial cell monolayers. CONCLUSIONS: The galactosyl receptor provides a valuable target for the development and use of synthetic ligands capable of disrupting endothelial cell-prostate cancer cell interaction, the first step in prostate cancer bone metastasis.

Animals↗
PubMed2000

Attachment of primary neonatal rat astrocytes to vitronectin is mediated by integrins alphavbeta5 and alpha8beta1: modulation by the type 1 plasminogen activator inhibitor.

Vitronectin is expressed in a cell-specific manner in the developing brain and concentrated in the brain during disease processes, such as germinal matrix hemorrhage and infarction, in which there is breakdown of the blood-brain barrier. In this study, we identified the integrin receptors that mediate attachment of primary neonatal rat astrocytes to vitronectin. Using fluorescent activated cell sorter and immunoprecipitation analyses, we established that the vitronectin receptor integrins alphavbeta5 and alpha8beta1, but not alphavbeta3, are expressed on neonatal rat astrocytes. Attachment of the neonatal astrocytes to vitronectin was inhibited (85%) in an additive manner by neutralizing anti-alphavbeta5 and anti-beta1 antibodies. Attachment to vitronectin was also inhibited in a dose-dependent manner by the type I plasminogen activator inhibitor (PAI-1), a serine protease inhibitor. Our data demonstrate that unstimulated primary neonatal rat astrocytes attach to vitronectin, utilizing integrins alphavbeta5 and alpha8beta1, and that this attachment is regulated by PAI-1.

Animals↗
PubMed2000

Expression of osteopontin messenger RNA and protein in rheumatoid arthritis: effects of osteopontin on the release of collagenase 1 from articular chondrocytes and synovial fibroblasts.

OBJECTIVE: Osteopontin (OPN) is an extracellular matrix protein that has been implicated in the interactions between tumor cells and host matrix, including those involved in invasion and spread of tumor cells. Because joint destruction in rheumatoid arthritis (RA) is mediated by the invasive growth of synovial tissue through its attachment to cartilage, we examined the expression of OPN in the synovia of patients with RA and the effect of OPN on the production of collagenase 1 in rheumatoid synovial fibroblasts and articular chondrocytes. METHODS: The expression of OPN messenger RNA (mRNA) and protein in synovia from 10 RA patients was examined by in situ hybridization and immunohistochemistry. Synovial fibroblasts from RA patients and articular chondrocytes from patients without joint disease were cultured in the presence of various concentrations of OPN, and levels of collagenase 1 in the culture supernatants were measured by enzyme-linked immunosorbent assay. RESULTS: The expression of OPN mRNA and protein was observed in 9 of 10 specimens obtained from patients with RA. OPN was expressed in the synovial lining and sublining layer and at the interface of cartilage and invading synovium. Double labeling revealed that the majority of OPN-expressing cells were positive for the fibroblast-specific enzyme prolyl 4-hydroxylase and negative for the macrophage marker CD68, while only a few, single OPN-expressing cells were positive for CD68 at sites of synovial invasion into cartilage. OPN staining was not observed in lymphocytic infiltrates or leukocyte common antigen (CD45)-positive cells. Three of 3 cultures of human articular chondrocytes secreted detectable basal amounts of collagenase, with a dose-dependent increase upon OPN stimulation, while synovial fibroblast cultures produced much lower levels of collagenase, with only 2 of 4 fibroblast cultures responding in a dose-dependent manner. CONCLUSION: These findings suggest that OPN produced by synovial fibroblasts in the synovial lining layer and at sites of cartilage invasion not only mediates attachment of these cells to cartilage, but also contributes to matrix degradation in RA by stimulating the secretion of collagenase 1 in articular chondrocytes.

Aged↗
PubMed2000

Somatic gene therapy for a neurodegenerative disease using microencapsulated recombinant cells.

Neurodegenerative diseases caused by lysosomal enzyme deficiencies are catastrophic illnesses with both peripheral organ and central nervous system abnormalities. The mucopolysaccharidosis type VII mouse with beta-glucuronidase deficiency was used to develop an alternate approach to gene therapy, in which a "universal" cell line engineered to secrete the missing enzyme is implanted directly into all recipients requiring the same enzyme replacement. The cells, though nonautologous, were rendered immunologically tolerable by protection in immunoisolating microcapsules. Since the blood-brain barrier impedes the passage of large molecules such as beta-glucuronidase, encapsulated cells producing beta-glucuronidase were introduced directly into the lateral ventricles of the brain. Based on this strategy, beta-glucuronidase was delivered throughout most of the central nervous system, reversing the histological pathology and reducing the previously elevated levels of lysosomal enzymes beta-hexosaminidase and alpha-galactosidase. The effectiveness of this approach was further demonstrated with improvements in the mutant circadian rhythm behavioral abnormalities. Compared to wild-type and heterozygous mice, the mutant mice had an unstable periodicity, fragmented activity, and a sixfold reduction in wheel running activity. After treatment, the mutant behavioral abnormalities were significantly improved with a more stable periodicity and a less fragmented pattern of activity. While the overall total activity level did not increase in the treated mutants, it did not show the deterioration observed in the sham-treated as well as in the untreated mutant mice. Hence, this alternative cell-based gene therapy demonstrates biochemical, histological, and behavioral efficacy and provides a potentially cost-effective and nonviral treatment applicable to all lysosomal storage diseases with neurological deficits.

Alginates↗
PubMed2000

Improvement of health outcomes after continued implementation of a clinical pathway for radical nephrectomy.

The clinical pathway is an important tool for outcome management. We evaluated the overall effects of the continued implementation of a clinical pathway for radical nephrectomy on the length of hospital stay, admission charges, and the quality of medical care. The data obtained from the second-year implementation (group 3) of the clinical pathway were compared with the data from the first-year implementation (group 2) and the year preceding implementation (group 1). Thirty-seven consecutive patients with renal cell carcinoma underwent radical nephrectomy in group 1, 47 in group 2, and 55 in group 3; all were enrolled in this study. The length of hospital stay, average admission charges, and 8 quality indicators were measured in these patients. We also evaluated the variances in the implementation of the clinical pathway. The mean length of stay decreased by 14.0% (P = 0.0048) in group 2, and by 15.8% (P= 0.0014) in group 3, when compared to group 1. The total admission charges significantly decreased by 19.0% (P = 0.001) in group 2, and by 27.9% (P < 0.0001) in group 3, compared to the charges for group 1. A continued decrease in charges for operation and anesthesia, laboratory, pharmacy, and others were found 2 years after implementation of the clinical pathway. Among the 8 quality indicators, 2 were continuously improved in the second-year implementation of the clinical pathway, 2 were improved significantly in the second-year implementation only, and 4 showed no significant change at all. Variances from the clinical pathway decreased significantly after continued implementation. Continued implementation of the clinical pathway for radical nephrectomy can improve a physician's practice continuously by decreasing the length of hospital stay, admission charges, and variances, and by improving quality. However, the improved results after implementation of the clinical pathway should be maintained carefully to assure good health care.

Adult↗