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PubMed2002

An analysis of advocacy: a collaborative essay.

OBJECTIVES: To review the development of advocacy and its influence on health policy from the perspective of AIDS, the American Cancer Society, the Cancer Leadership Council, and the Patient Advocacy Foundation. DATA SOURCES: Published articles, news articles, books and personal experience. CONCLUSIONS: Advocacy on behalf of patients in the health care arena is a powerful force in modern life. Advocacy organizations have been influential in the development of health policy. IMPLICATIONS FOR NURSING PRACTICE: There are a variety of advocacy organizations in which nurses can commit their energies in the support of advocacy.

Acquired Immunodeficiency Syndrome↗
PubMed1995

Hormonal response of primary hepatocytes of the clawed toad, Xenopus laevis.

Freshly isolated hepatocytes of the clawed toad, Xenopus laevis, were cultured for at least 3 days. The viability of the cells was characterized using staining and biochemical methods. In particular, the glucose and glycogen balance was tested. After culture for 16-20 hrs, the cells were subjected to hormonal treatment. Both adrenaline and arginine vasotocin stimulated the release of glucose in a dose dependent manner. 10(-6) M concentrations were strongly effective. The determination of the glycogen balance made it clear that the glucose release is mainly due to glycogenolysis. Using receptor antagonists and agonists, it has been shown that the effect of adrenaline is clearly mediated by beta-type receptors. Arginine vasotocin stimulated glycogenolysis via a type of receptor which is similar to the V2-receptor of mammals. This means that cAMP is involved in the response to both types of hormones which is in contrast to that which is known about the effect of nonapeptides on the liver of mammals.

Animals↗
PubMed2000

Low caloric expenditure in cardiac rehabilitation.

BACKGROUND: Total physical activity energy expenditure is a determinant of weight loss and risk factor modification in adults. There has been very little study of physical activity energy expenditure in cardiac rehabilitation populations. METHODS: Exercise-related energy expenditure was calculated in 112 patients with coronary artery disease in an outpatient cardiac rehabilitation program. Gross energy expenditure was estimated with the heart rate/oxygen consumption relation as measured during metabolic exercise testing with expired gas analysis. RESULTS: The average exercise training energy expenditure (ETEE) per cardiac rehabilitation exercise session was quite low at 270 +/- 112 kcal. Baseline fitness level (peak oxygen consumption), body weight, total exercise duration per session, age, and body mass index were all significant determinants of ETEE (r = 0.56 to -0.37, all P <.01). Additionally, patients who had undergone coronary bypass surgery and patients with medical comorbidities expended significantly fewer calories during exercise. In women, there was a relation between ETEE and change in total and LDL cholesterol (r = -0.43 and -0.45, respectively), although no such relation was observed in men. CONCLUSION: Cardiac rehabilitation exercise training, as currently structured, burns surprisingly few calories and has little impact in the short term (3 months) on measures of obesity and lipid risk factors. Alternative training programs should be considered to maximize caloric expenditure and modify specific risk factors such as obesity and dyslipidemia.

Aged↗
PubMed2002

Determinants of disability in older coronary patients.

BACKGROUND: Patient-reported physical function is a major component of disability determinations and an important contributor to health-related quality of life. Prior studies of coronary disability have shown a surprisingly poor correlation between real-life activity profile and exercise capacity measured on the treadmill. The goal of the current investigation was to evaluate the relative importance of medical factors, sex, fitness-related measures, and psychologic factors as determinants of patient-reported physical function score in older persons with established coronary heart disease (CHD). METHODS: Determinants of disability were studied in 51 community-dwelling patients >65 years old (71 +/- 5 years, range 65-83 years) with established chronic CHD. Patient-reported physical function score (scaled 0-100) was measured by the Medical Outcomes Study Short Form physical function section. Independent variables included clinical and demographic data, treadmill testing, rest and exercise echocardiography, measures of body composition, strength, aerobic fitness, and a depression score. RESULTS: Patients with a diagnosis of myocardial infarction had a lower physical function score than did patients with other CHD diagnoses (68 +/- 19 vs 82 +/- 22, P <.05). Univariate predictors of patient-reported physical function score included peak aerobic capacity (R = 0.62), treadmill test duration (R = 0.61), depression score (R = -0.60), handgrip strength (R = 0.42), and comorbidity score (R = -0.39). Peak aerobic capacity (R2 = 0.38) and depression score (cumulative R2 = 0.60) were the best independent predictors of physical function. Women had lower physical function scores than men (64 +/- 22 vs 78 +/- 20, P <.05) despite a similar age, diagnostic distribution, depression score, and comorbidity score. Resting left ventricular ejection fraction was not a predictor of physical function score. CONCLUSIONS: Peak aerobic capacity and depression score were the best independent predictors of patient-reported physical function score in older coronary patients. These data focus on the potential for exercise training and treatment of mental depression to prevent and treat coronary disability in older coronary patients.

Absorptiometry, Photon↗
PubMed2003

Is intralesional injection of OK-432 effective in the treatment of lymphangioma in children?

BACKGROUND: Intralesional injection of OK-432 has been proposed as an effective treatment of lymphangioma. The aim of this study was to review our experience with OK-432 injection of lymphangioma and to identify factors associated with successful outcome. METHODS: We made a case note review of 19 children who received OK-432 injection. Median duration of follow-up was 17 months. RESULTS: Lesions were diagnosed antenatally in 4 children, at birth in 4 children, and between 1 month and 11 years in the remainder. Anatomic locations were head/neck in 14, axilla in 1, and multiple locations in 4. Median number of injections per child was 2 (range, 1 to 5). Disappearance of the lesion was achieved after OK-432 injection in 2 patients (11%) and a marked reduction in 5 (26%); all these lesions were in the head and neck. Lesions larger than 5 cm and those outside the head and neck region did not respond well to OK-432 injection. Fourteen children (74%) required surgical excision after injection. Complications of OK-432 injection included partial tracheal obstruction, fever, local inflammatory response, and abscess formation. CONCLUSIONS: OK-432 injection was effective in approximately one third of children with lymphangioma. Lesions outside the head and neck and those larger than 5 cm are unlikely to respond to this therapy. Injection of lymphangioma surrounding the airways may be hazardous.

Antineoplastic Agents↗
PubMed1981

Complete amino acid sequence of beta-tubulin from porcine brain.

The primary structure of porcine brain beta-tubulin was determined by automated and manual Edman degradation of six sets of overlapping peptides. The protein consists of 445 amino acid residues and has a minimum of six positions that are heterogeneous, indicating at least two beta-tubulins in porcine brain. Comparison of the optimally aligned sequences of alpha-tubulin and beta-tubulin indicates that 41% of their primary structures are identical. A region rich in glycyl residues is similar both in sequence and predicted secondary structure to the phosphate binding loop of several nucleotide binding enzymes. beta-Tubulin contains a highly acidic COOH-terminal region that resembles the NH2-terminus of troponin T.

Amino Acid Sequence↗
PubMed1985

Carboxyl-terminal domain of the Epstein-Barr virus nuclear antigen is highly immunogenic in man.

The carboxyl-terminal one-third of the Epstein-Barr virus nuclear antigen (EBNA-1) encoded by the BamHI restriction fragment K was synthesized in Escherichia coli by use of a high-expression plasmid. The resultant 28-kDa EBNA fusion polypeptide, comprising 5-10% of the total soluble bacterial protein, was purified to apparent homogeneity by phosphocellulose and hydroxylapatite column chromatography. Both rabbit monospecific antibodies and mouse monoclonal antibodies against 28-kDa EBNA gave nuclear immunofluorescence staining on Epstein-Barr virus (EBV)-infected lymphoblastoid cell lines and recognized the appropriate intact EBNA polypeptide bands on immunoblots. An ELISA with the purified 28-kDa EBNA as antigen was used to quantitate anti-EBNA antibody in human serum samples. The ELISA method was approximately 100-fold more sensitive than the classical anticomplement immunofluorescence assay. Anti-EBNA antibody was detected in sera from 100% of normal individuals who were seropositive for the viral capsid antigen, and low anti-EBNA titers were detected in serum from most patients with acute infectious mononucleosis. The assay gave the expected pattern of titers in sera from patients with rheumatoid arthritis, Burkitt lymphoma, or nasopharyngeal carcinoma, thus confirming the validity of this purified reagent for assessing EBNA antibody status. Approximately 10% of normal individuals and rheumatoid arthritis patients had anti-EBNA titers as high as those seen in nasopharyngeal carcinoma patients. In these high-titer individuals, greater than 1% of the total IgG are antibodies that recognize 28-kDa EBNA, which indicates that the carboxyl-terminal domain of EBNA is highly immunogenic.

Amino Acid Sequence↗
PubMed1996

Effect of age on in vivo rates of mitochondrial protein synthesis in human skeletal muscle.

A progressive decline in muscle performance in the rapidly expanding aging population is causing a dramatic increase in disability and health care costs. A decrease in muscle endurance capacity due to mitochondrial decay likely contributes to this decline in muscle performance. We developed a novel stable isotope technique to measure in vivo rates of mitochondrial protein synthesis in human skeletal muscle using needle biopsy samples and applied this technique to elucidate a potential mechanism for the age-related decline in the mitochondrial content and function of skeletal muscle. The fractional rate of muscle mitochondrial protein synthesis in young humans (24 +/- 1 year) was 0.081 +/- 0.004%.h-1, and this rate declined to 0.047 +/- 0.005%.h-1 by middle age (54 +/- 1 year; P < 0.01). No further decline in the rate of mitochondrial protein synthesis (0.051 +/- 0.004%.h-1) occurred with advancing age (73 +/- 2 years). The mitochondrial synthesis rate was about 95% higher than that of mixed protein in the young, whereas it was approximately 35% higher in the middle-aged and elderly subjects. In addition, decreasing activities of mitochondrial enzymes were observed in muscle homogenates (cytochrome c oxidase and citrate synthase) and in isolated mitochondria (citrate synthase) with increasing age, indicating declines in muscle oxidative capacity and mitochondrial function, respectively. The decrease in the rates of mitochondrial protein synthesis is likely to be responsible for this decline in muscle oxidative capacity and mitochondrial function. These changes in muscle mitochondrial protein metabolism may contribute to the age-related decline in aerobic capacity and muscle performance.

Adult↗
PubMed1995

An acute phase response factor/NF-kappa B site downstream of the junB gene that mediates responsiveness to interleukin-6 in a murine plasmacytoma.

The immediate early gene, junB, is induced by interleukin-6 (IL-6) in plasmacytomas. In order to identify enhancers that mediate this effect, we cloned upstream and downstream sequences flanking the gene into a luciferase reporter gene vector containing the junB promoter and evaluated the IL-6 inducibility of these sequences by transient expression in an IL-6-dependent plasmacytoma cell line. Although a 6.5-kilobase fragment of upstream flanking sequence did not increase the IL-6 inducibility of the junB promoter, a 222-base pair fragment was identified in 2.1 kilobases of down-stream flanking sequence that both up-regulates the promoter and confers inducibility by IL-6. Point mutation of an acute phase response factor (APRF) site within this region significantly reduced up-regulation of the promoter in cells grown continuously in IL-6, as well as inducibility upon restimulation of cells with IL-6 after withdrawal from the growth factor. Point mutation of an NF-kappa B site sharing five nucleotides with the APRF site reduced up-regulation of the promoter but not inducibility by IL-6, whereas mutation of two other NF-kappa B sites in the 222-base pair fragment had no effect on expression. Western blotting of nuclear proteins purified by DNA affinity chromatography revealed inducible binding of Stat3 and constitutive binding of NF-kappa B p65 to the APRF/NF-kappa B site.

Animals↗
PubMed1997

Studies on intracellular translocation of apolipoprotein B in a permeabilized HepG2 system.

Recent evidence suggests that the rate of apolipoprotein B-100 (apoB) translocation may be a key regulatory point in the production of apoB-containing lipoproteins. We have developed an in vitro system to measure the translocation rate of apoB in HepG2 cells. Intact cells were initially pretreated with oleate and N-acetyl-Leu-Leu-norleucinal to maximize the translocation rate while minimizing degradation. Cells were pulsed with [35S]methionine, chased (5-30 min), and then permeabilized with digitonin (75 microg/ml). Permeabilized cells were incubated with or without trypsin (200 microg/ml) for 10 min, and digestion was halted with soybean trypsin inhibitor (2 mg/ml). The rate of translocation was determined by comparing the amount of immunoprecipitable intact apoB in trypsin-treated cells with that in control cells at each time point. Under these conditions, two control proteins, alpha1-antitrypsin and transferrin, were fully protected from trypsin digestion, confirming the integrity of the secretory pathway in permeabilized cells. The percentage of apoB translocated steadily increased from 36% after 5 min to 71% after a 30-min chase (mean percentage, n = 3). A characteristic apoB fragmentation pattern resulted from trypsin digestion, and protected fragments of various size including N-terminal 60-70-kDa fragments were identified. Subcellular fractionation of the cells confirmed that the apoB pool protected from trypsin digestion was luminal in nature, confirming its translocation. ApoB translocation was significantly increased in oleate-treated cells compared with untreated cells. Inhibition of peptidylprolyl isomerase through the use of cyclosporin A and disruption of disulfide bond formation using dithiothreitol reduced the percentage of translocated apoB by 37 and 63%, respectively. Dithiothreitol induced specific changes in the pattern of protected apoB fragments, suggesting a conformational change in apoB that may hinder its translocation. Inhibition of N-linked glycosylation with tunicamycin did not significantly alter the rate of apoB translocation but appeared to stimulate its degradation. Together, the data suggest that the rate of apoB translocation across the membrane of the ER is determined by both lipid availability as well as the correct conformation of nascent apoB molecules.

Apolipoproteins B↗
PubMed1997

Apolipoprotein B is intracellularly associated with an ER-60 protease homologue in HepG2 cells.

Two ALLN (N-acetyl-leucyl-leucyl-norleucinal)-sensitive endoplasmic reticulum (ER)-localized proteases (ER-60 and ER-72) were recently purified from rat liver. We used an antibody to rat ER-60 to investigate the possible role of this protease in apolipoprotein B (apoB) degradation. First, immunoprecipitation and immunoblotting experiments with the anti-rat ER-60 antibody suggested that HepG2 cells contain a homologue of ER-60 with an approximate molecular mass of 58-60 kDa. The ER-60 homologue was mostly associated with the luminal contents of HepG2 microsomes. Evidence from co-immunoprecipitation and cross-linking experiments appear to suggest that the ER-60 homologue in HepG2 cells is associated with apoB intracellularly. A small pool of apoB was recovered when HepG2 lysates were subjected to immunoprecipitation with anti-rat ER-60 antibody followed by a second immunoprecipitation with anti-apoB antibody. Furthermore, cross-linking of permeabilized cells with dithiobis(succinimidylpropionate) further demonstrated association of apoB with the ER-60 homologue in HepG2 cells. Three polypeptides with molecular masses of 78, 66, and 50 kDa were consistently found to be associated with apoB as well as the 58-kDa ER-60 homologue. The 78-kDa protein associated with both apoB and ER-60 appeared to represent immunoglobulin heavy chain-binding protein (BiP) based on immunoprecipitation with a monoclonal antibody. Cross-linking and immunoblotting experiments suggested the association of the 78-kDa BiP with both the 58-kDa ER-60 homologue as well as the 550-kDa apoB. In summary, the data suggests that HepG2 cells contain a 58-kDa protein which is homologous to the rat liver ER-60 in size, antigenecity, and intracellular localization. The ER-60 homologue in HepG2 cells appears to be closely associated with apoB, as well as other proteins possibly representing ER chaperones such as BiP. We hypothesize that the ER-60 homologue may be involved in the degradation of apoB in the ER lumen of HepG2 cells.

Animals↗
PubMed1997

Intracellular assembly and degradation of apolipoprotein B-100-containing lipoproteins in digitonin-permeabilized HEP G2 cells.

Permeabilized Hep G2 cells have been used to investigate the turnover of apolipoprotein B-100 (apoB-100). When such cells were chased in the presence of buffer, there was no biosynthesis of apoB-100, nor was the protein secreted from the cells. Thus the turnover of apoB-100 in these cells reflected the posttranslational degradation of the protein. Pulse-chase studies indicated that apoB-100 was degraded both when associated with the membrane and when present as lipoproteins in the secretory pathway. Neither albumin nor alpha1-antitrypsin showed any significant posttranslational intracellular degradation under the same condition. The kinetics for the turnover of apoB-100 in the luminal content differed from that of apoB-100 that was associated with the microsomal membrane. Moreover, while the degradation of the luminal apoB-100 was inhibited by N-acetyl-leucyl-leucyl-norleucinal (ALLN), this was not the case for the membrane-associated protein. Together these results suggest the existence of different pathways for the degradation of luminal apoB-100 and membrane-associated apoB-100. This was further supported by results from pulse-chase studies in intact cells, showing that ALLN increased the amount of radioactive apoB-100 that associated with the microsomal membrane during the pulse-labeling of the cells. However, ALLN did not influence the rate of turnover of the membrane-associated apoB-100. The presence of an ATP-generating system during the chase of the permeabilized cells prevented the disappearance of pulse-labeled apoB-100 from the luminal lipoprotein-associated pool. The ATP-generating system combined with cytosol protected the total apoB-100 in the system from being degraded. The cells cultured in the presence of oleic acid and chased after permeabilization in the presence of cytosol and the ATP-generating system showed an increase in the amount of apoB-100 present on dense ("high density lipoprotein-like") particles. This increase was linear during the time investigated (i. e. from 0 to 2 h chase) and independent of protein biosynthesis. Our results indicate that the dense particle was generated by a redistribution of apoB-100 within the secretory pathway and that it most likely was assembled from the membrane- associated form of apoB-100. These results indicate that the release of apoB-100 from this membrane-associated form to the microsomal lumen is dependent on cytosolic factors and a source of metabolic energy.

Apolipoproteins B↗