An analysis of the pragmatic consequences of holism for nursing.
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Biomedical subjects
Publications and source records attributed to C E Allen.
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The effect of antimicrobial supplementation of pigs on the capacity of their sera to influence proliferation and protein turnover in cultured muscle cells was evaluated. Mitogenic activity of sera increased when pigs were fed ASP250 (P less than .005) or carbadox (P less than .001), whereas the mitogenic activity of serum from pigs receiving the basal diet remained unchanged (P = .5). Additionally, sera from ASP250-fed pigs significantly decreased (P less than .001) total cellular protein degradation compared with sera obtained from the same pigs prior to supplementation. Neither ASP250 nor carbadox stimulated proliferation of myogenic cells when added to the culture media. Inclusion of ASP250 in swine diets altered the composition of their sera in a way that stimulated muscle cell proliferation and reduced the rate of protein degradation in cultured myogenic cells. Likewise, the inclusion of carbadox in swine diets increased the ability of their sera to stimulate cultured muscle cell proliferation.
Sera obtained from pigs before and after subtherapeutic levels of ASP250 supplementation (pre and post serum pools) have been subjected to comparative fractionation by using gel filtration and affinity chromatography on immobilized Cibacron Blue F3G-A. Comparable serum fractions obtained from pre- and post-ASP250 blood sera were assayed in muscle cell culture bioassays designed to measure their effect on proliferation. Pre- and post-ASP250 sera were subjected to gel filtration and divided into the following fractions: fraction 1, Kav less than .17; fraction 2, Kav = .17 to .41; fraction 3, Kav = .41 to .59. Post-ASP250 fractions 2 and 3 increased proliferation rate in cultured muscle cells to a greater extent than comparable pre-ASP250 fractions (P less than .001). Chromatography of fraction 3 on immobilized Cibacron Blue F3G-A showed that both pre- and post-ASP250 fraction 3 contained a putative inhibitor of myogenic cell proliferation as well as mitogenic factors. However, negative growth factor activity was greater in pre-ASP250 fraction 3 than in post-ASP250 fraction 3 (P less than .05). Additionally, positive growth factor activity was lower in pre-ASP250 fraction 3 than in post-ASP250 fraction 3 (P less than .05). These data suggest that levels and(or) activities of both positive and negative muscle growth factors in serum may be altered by the addition of antimicrobials to the diets of growing pigs.
Sera from pigs fasted as little as 24 h appears to contain a factor(s) that inhibits proliferation of myogenic cells in culture. An inhibitor of myogenic cell proliferation has been partially purified from this sera by using a combination of gel filtration and immunoaffinity chromatography. The inhibitory activity elutes from a Sephacryl S-300 column at a Kav (elution minus void volume divided by total minus void column volume) between .41 and .59. Proteins banding at 76 and 67 kilodaltons appear to predominate on sodium dodecyl sulfate polyacrylamide gels of this fraction. Small quantities of each of these proteins were electrophoretically purified and used to elicit production of anti-76 and anti-67 immunoglobulin G in rabbits. These antibodies were used to prepare anti-76 and anti-67 column was particularly useful in isolating the inhibitor because it removed mitogens that made detection of the inhibitory activity difficult. The partially purified inhibitor inhibits proliferation of L6 myogenic cells in a concentration-dependent manner. On sodium dodecyl sulfate polyacrylamide gels, the predominant proteins in the inhibitor fraction band at approximately 63 and 61 kilodaltons. Inhibitors of myogenic cell proliferation may play an important role in balancing the effects of positive growth factors.
This study assessed whether participation in a structured career decision-making course would enhance the career planning of 42 final semester associate degree nursing students. Levels of career planning were measured by the Career Planning Scale (CPS) (Super, Thompson, Lindman, Jordaan, & Myers, 1982), and the Nursing Career Development Inventory (NCDI) (Savickas, 1984). Subjects were randomly assigned to either an experimental or control group. The experimental group received a four-week career decision-making course, which included self-assessment of values, interests, and skills, and information on occupational opportunities in nursing. An ANOVA on the change scores from pretest to post-test revealed significance between the groups on the CPS (p = .002), and on the NCDI (p less than .00001). The experimental group progressed much more in career planning. All subjects were found to have lower levels of career planning than the average college student at pretest. Intercorrelational data and multiple regression analyses indicated that individuals who had worked in a nursing-related field had higher levels of career planning. Overall, the course emerged as being effective in enhancing the career planning of nursing students.
The effects of fasting on the ability of swine serum to affect proliferation, protein synthesis and protein degradation in L6 myoblast cell culture bioassays were evaluated. Barrows (15 to 20 kg) were fitted with jugular catheters. Blood samples were collected at four evenly spaced intervals between 0800 and 1700 on collection days. Prefast blood samples were obtained on d 1 and 2 of the study, after which pigs were subjected to a 5-d fast. Fasted samples were obtained on the 1st, 3rd and 5th d of the fast (d 3, 5 and 7 of the study). Serum from each collection day was pooled and tested in the proliferation bioassay for each pig. Prefast and fasted serum pools were formed by pooling prefast days (1 and 2) or fasted days (3, 5 and 7), respectively, from all pigs in a study. These pools were tested in the proliferation and protein turnover bioassays as well as in a Somatomedin-C (SmC) radioimmunoassay. Serum from the fasted collection days showed a decrease in mitogenic activity compared with serum from the two prefast days (P less than .001). At high concentrations, sera obtained from fasted pigs inhibited muscle cell proliferation (P less than .001). Additionally, adding fasted serum to control swine serum (CSS) inhibited the mitogenic activity of CSS in a dose-dependent manner (P less than .025). Therefore, fasted sera showed a decreased ability to promote muscle cell proliferation and, in addition, appeared to contain a factor(s) that inhibits muscle cell proliferation. Fasted serum also caused a 21.6% increase in protein degradation compared with prefast serum.(ABSTRACT TRUNCATED AT 250 WORDS)
We have developed a statistically standardized bioassay for quantifying the effect of swine serum on the proliferation rate of cultured L6 myogenic cells. The intra-assay coefficient of variation for this assay is 2.5%. Over 29 experiments, the relationship between the assays response to 2.5% control swine serum and its response to 2.5% serum plus 10(-7) M insulin is linear (r2 = .9). This relationship can be used to adjust experimental data obtained in different experiment to a common control value so that valid inter-assay comparisons can be made. The inter-assay coefficient of variation is reduced four- to five fold by this adjustment procedure. We believe this standardized assay provides a useful system for identifying and isolating unknown growth factors that affect muscle growth rate in an economically important species.
The proliferation-promoting activity of sera obtained from pigs before and after porcine growth hormone injections was tested in a muscle cell culture bioassay. For 3 d, purified porcine growth hormone (pGH) was administered by intramuscular injection to crossbred barrows. Two levels of pGH were administered: 18 micrograms pGH X kg-1 body weight X d-1 (low dose) or 143 micrograms pGH X kg-1 body weight X d-1 (high dose). Multiple blood samples were withdrawn from jugular catheters for 3 d prior to the injection, during the injection period and for 6 d after the last injection. Although serum pGH levels in low-dose pigs were raised from two to three times pre-injection levels, there was no significant change in serum proliferation-promoting activity or somatomedin-C (SmC), insulin or cortisol levels during or after administration of pGH. In contrast, the proliferation-promoting activity of sera obtained during and after the high-dose pGH injections was higher (P less than .005) than the pre-injection levels. Serum pGH levels were increased approximately 30-fold by 4 h after each injection, and increases in SmC levels were observed 10 to 16 h after the pGH injection. During the injection period SmC levels increased from 1.7 to 4 times pre-injection levels. Insulin and cortisol levels did not change significantly during the 3-d treatment period. We believe that this muscle cell culture bioassay system will be a useful addition to traditional radioimmunoassays and whole animal studies in elucidating the mode of action of pGH in pituitary-intact swine.
The purpose of this study was to determine if the metabolic response to obesity and to pair feeding of obese Zucker rats to lean Zucker rats was similar across skeletal muscles. Oxidation of glucose, palmitate and isoleucine was studied in muscle strips in vitro using appropriate 14- carbon substrates as tracers. The plantaris muscle was subjected to histochemical analyses using an alkaline actomyosin ATPase, NADH-tetrazolium reductase and an oil red 0 stain. Soleus muscles from both ad libitum and pair fed obese rats oxidized less glucose to CO2, but released similar amounts of lactate when compared to the soleus muscles of lean rats. Oxidation of glucose was similar in the extensor digitorum longus (EDL) muscle of ad libitum fed obese rats, but lower when pair fed to the intake of lean rats. No differences were apparent in palmitate oxidation to CO2 or in incorporation into lipid (both soleus and EDL muscles), except in the EDL muscle of pair-fed obese rats which exhibited a higher rate for palmitate metabolism when compared with lean rats. Isoleucine oxidation to CO2 was higher in the EDL and plantaris muscles, but similar in the soleus muscle of ad libitum-fed obese rats when compared with lean rats. The magnitude of the difference in isoleucine oxidation was similar when the obese rats were pair fed. No differences in the percentage of plantaris muscle fibers sensitive to alkaline ATPase staining were observed. The plantaris muscle of obese rats, contained a higher proportion of oxidative fibers. These results indicate the great risk in generalizing about metabolic activity of the whole skeletal muscle mass based on observations made on one, or even two, distinct muscles in this animal model. Also, pair feeding of obese to lean Zucker rats did not result in uniform changes in metabolism between muscles of the obese rats.
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Glucagon has been shown to lower blood lipids and to decrease food intake and body weight in short-term studies in man and animals. There is evidence of decreased secretion of glucagon in human obesity. The Zucker obese rat suffers from a genetic type of obesity and has an absolute reduction in circulating glucagon concentration. The effect of long-term administration of glucagon on the body weight in obese Zucker rats was studied. Glucagon caused a marked (-20%) reduction of body weight in obese Zucker rats with no change in feed intake. Urine glucose, urea nitrogen, creatinine, and ketone content, as well as serum triglyceride, cholesterol, alkaline phosphatase, creatinine, and insulin levels remained unchanged. Weights of perirenal fat, kidneys, and heart also remained unchanged. However, glucagon injection in obese Zucker rats caused significant decrease in serum glucose, and increases in SGOT, liver weight, and liver lipid and glycogen content. Further investigations are needed concerning the safety of chronic glucagon administration for weight control.
Pituitary cells were isolated from lean and obese Zucker rats and compared with the use of two approaches. The first approach was to evaluate the capacity of an equal number of pituitary cells to stimulate growth in hypophysectomized rats. The rats implanted with lean pituitary cells grew at a similar rate as rats implanted with obese pituitary cells. Body composition was also determined to be similar in those rats receiving lean and obese rat pituitary cells. The second approach was to evaluate the in vitro secretory capacity of rat pituitary cells when placed in a superfusion system. Basal and stimulated growth hormone release was the same for lean and obese rat pituitary cells. These data support the hypothesis that the low level of serum growth hormone found in the Zucker obese rat is the result of a hypothalamic disorder and not a pituitary cell defect.
Experiments were conducted in pregnant pigs to determine the influence of alloxan diabetes and maternal fasting on fetal development. Maternal fasting and alloxan diabetes both increased adipose tissue thickness in fetuses at 112 days of gestation without altering body weight. Body fat was increased quantitatively only in the fetuses from the diabetic pigs (FDP). Apparently, different factors were affecting the structural development of adipose tissue and the actual storage of lipid. Fetal and maternal hepatic fatty acid synthesis were unaffected by treatments. Maternal subcutaneous adipose fatty acid synthesis were unaffected by treatments. Maternal subcutaneous adipose fatty acid synthesis was depressed by 75% in both fasted and diabetic dams while subcutaneous adipose tissue lipogenesis was increased 40-fold in the FDP. Enzymes normally associated with lipogenesis (shunt enzymes) were also affected in a similar fashion. These observations support the concept that fetal adipose de novo fatty acid synthesis is stimulated by diabetic pregnancies and is a primary mechanism by which increased lipid accumulates in the fetus.
Adipose tissue slices were prepared from middle subcutaneous or perirenal adipose tissue excised from pigs of different ages (and obesity) and incubated with [U-14C]glucose. After incubation, the slices were fixed with osmium tetroxide and separated into diameter ranges of 20--63, 63--102, and 102--153 microgram, respectively. Following determination of cell size and number, the fixed adipocytes were decolorized with H2O2 prior to quantification of glucose conversion to total lipid, glyceride fatty acids, glycerideglycerol, and CO2. Glucose conversion to total lipid or CO2 was unaffected by the presence of purified porcine insulin (0, 10, 100, 1000, and 100,000 microM/ml). Within animals, adipocytes of different sizes were not different with regard to insulin sensitivity. Within a weight (age) group, conversion of glucose to total lipid (insulin present) or to glyceride fatty acids and glyceride-glycerol (insulin absent) per cell was significantly greater in large adipocytes compared to small adipocytes, regardless of the group examined. With increasing weight or age, there was a markedly decreased conversion of glucose to total lipid and glyceride fatty acids among adipocytes of similar size within a cell-size fraction. The diminution in glucose metabolism was greater (as a percentage) in 20--63 microgram adipocytes than for 63--102 or 102--153 microgram adipocytes. However, for all cell-size fractions there was a marked decrease in glucose conversion to fatty acids. Glyceride-glycerol synthesis was impaired in adipocytes from older pigs, but the decrease was less than observed for glyceride fatty acid synthesis.
The effects of dietary vitamin E-depletion and repletion on the cyclooxygenase activity was studied in the semitendinosus muscle of rabbits. The prostaglandin (PG) cyclooxygenase system in rabbit semitendinosus muscle was characterized and found to depend on reduced glutathione and 1-epinephrine as cofactors. Skeletal muscle cyclooxygenase generates PGE2 and PGF2 alpha at a ratio approximately equal to one. Weanling New Zealand white rabbits were fed a vitamin E-deficient diet for 4 to 5 weeks. Controls received 50 mg dl-alpha-tocopherol acetate twice weekly. Vitamin E deficiency caused a significant reduction in cyclooxygenase activity but did not change the PGE2/PGF2 alpha ratio. Oral supplementation of tocopherol acetate promptly returned the cyclooxygenase activity back to the control values within 48 hours. The decreased cyclooxygenase activity explains in part the increased level of arachidonic acid in skeletal muscle phospholipid previously reported in this laboratory. The possible involvement of decreased prostaglandin endoperoxides with platelet aggregation in vitamin E deficiency is discussed.
The key enzyme controlling prostaglandin (PG) catabolism, 15-hydroxyprostaglandin dehydrogenase (PGDH), was characterized in rabbit tissues. The apparent Michaelis constant (Km) using PGE2 as substrate was found to be 5.3, 4.0, 4.0 and 7.1 microM for semitendinosus and soleus muscles, heart and kidney, respectively. The effect of dietary vitamin E depletion and repletion on the PGDH activity in these tissues was studied. Vitamin E deficiency caused an elevation of PGDH activity in rabbit skeletal muscles but not in the heart and kidney. Oral supplementation of tocopherol acetate to the deficient animals did not affect the skeletal muscle PGDH activity. A long period of refeeding (30 days) was required to suppress the elevated PGDH level to the control values. The data indicates a higher turnover of the PGs in the vitamin E-deficient rabbit skeletal muscles. The significance of such a change in connection to prostaglandin metabolism is discussed.