History of the meat animal evaluation contest: a pedagogical stimulant.

A century ago students were exposed to livestock judging and meat judging, though each was taught as an independent entity. Fifty years ago universities started combining subjects involving the evaluation process, whether characteristics involved traits of the live animal or those related to meat value. Universities developed a meat animal evaluation contest (MAEC) that included breeding livestock, market livestock, and meat products. Using production records, students culled, ranked, priced, and answered questions about breeding and market cattle, swine, and sheep. For market livestock, ranks and values were scored on carcass data after the livestock were harvested. Students graded, ranked, answered questions, and priced meat products. A communications component involved students being given a problem to be discussed as a group presentation. In 1964, the first MAEC was conducted at Rath Packing Co., Waterloo, IA, and included 40 students. In 1967, the contest was held at The Farmbest Co. and IBP of Denison, IA, and included 87 students. In 1968, the MAEC moved to the Knights of Ak-Sar-Ben, Omaha, NE, and by 1988, 187 students (22 universities) competed. In 1995, the MAEC moved to the United Stockyards Co., St. Joseph, MO. Starting in 2004, it moved to various universities (South Dakota State University, Oklahoma State University, University of Nebraska, and Texas Tech University). The MAEC has stimulated students to better learn and understand the details of meat animal evaluation and has encouraged the development of evaluation courses as well as satellite and symposia programs. To date, over 6,000 students representing 40 universities have participated.

Preregistration nursing education in Australia, New Zealand, the United Kingdom, and the United States of America.

The debate concerning nurses' diverse entry into practice was enlivened in 1995, when the American Nurses Association reaffirmed its contention that a baccalaureate degree was necessary for professional nursing practice. This debate may be informed by an appreciation of the educational routes taken by other countries that have changed from hospital-based to college-based nursing education. This paper describes and analyzes preregistration nursing education in Australia, New Zealand, the United Kingdom, and the United States, from the late nineteenth century to the present. Nurses in Australia and New Zealand are currently educated entirely at the baccalaureate level. In the United Kingdom, nursing education is in the process of becoming completely university-based, resulting in a diploma or degree. In the United States, the majority of nurses graduate from two-year associate degree programs. This level of education, briefer than in the other countries described, potentially limits nurses' professional contributions.

Mitochondrial abnormalities in Alzheimer's disease.

The finding that oxidative damage, including that to nucleic acids, in Alzheimer's disease is primarily limited to the cytoplasm of susceptible neuronal populations suggests that mitochondrial abnormalities might be part of the spectrum of chronic oxidative stress of Alzheimer's disease. In this study, we used in situ hybridization to mitochondrial DNA (mtDNA), immunocytochemistry of cytochrome oxidase, and morphometry of electron micrographs of biopsy specimens to determine whether there are mitochondrial abnormalities in Alzheimer's disease and their relationship to oxidative damage marked by 8-hydroxyguanosine and nitrotyrosine. We found that the same neurons showing increased oxidative damage in Alzheimer's disease have a striking and significant increase in mtDNA and cytochrome oxidase. Surprisingly, much of the mtDNA and cytochrome oxidase is found in the neuronal cytoplasm and in the case of mtDNA, the vacuoles associated with lipofuscin. Morphometric analysis showed that mitochondria are significantly reduced in Alzheimer's disease. The relationship shown here between the site and extent of mitochondrial abnormalities and oxidative damage suggests an intimate and early association between these features in Alzheimer's disease.

Uridine phosphorylase association with vimentin. Intracellular distribution and localization.

Uridine phosphorylase (UPase), a key enzyme in the pyrimidine salvage pathway, is associated with the intermediate filament protein vimentin, in NIH 3T3 fibroblasts and colon 26 cells. Affinity chromatography was utilized to purify UPase from colon 26 and NIH 3T3 cells using the uridine phosphorylase inhibitor 5'-amino benzylacyclouridine linked to an agarose matrix. Vimentin copurification with UPase was confirmed using both Western blot analysis and MALDI-MS methods. Separation of cytosolic proteins using gel filtration chromatography yields a high molecular weight complex containing UPase and vimentin. Purified recombinant UPase and recombinant vimentin were shown to bind in vitro with an affinity of 120 pm and a stoichiometry of 1:2. Immunofluorescence techniques confirm that UPase is associated with vimentin in both NIH 3T3 and colon 26 cells and that depolymerization of the microtubule system using nocodazole results in UPase remaining associated with the collapsed intermediate filament, vimentin. Our data demonstrate that UPase is associated with both the soluble and insoluble pools of vimentin. Approximately 60-70% of the total UPase exists in the cytosol as a soluble protein. Sequential extraction of NIH 3T3 or colon 26 cells liberates an additional 30-40% UPase activity associated with a detergent extractable fraction. All pools of UPase have been shown to possess enzymatic activity. We demonstrate for the first time that UPase is associated with vimentin and the existence of an enzymatically active cytoskeleton-associated UPase.

Characterization of a baculovirus-encoded protein that is associated with infected-cell membranes and budded virions.

Two types of envelope fusion proteins have been identified in lepidopteran baculoviruses. GP64 is found in Autographa californica multinucleocapsid nucleopolyhedrovirus, Orgyia pseudotsugata multinucleocapsid nucleopolyhedrovirus (OpMNPV), and other relatively closely related viruses, while Lymantria dispar multinucleocapsid nucleopolyhedrovirus (LdMNPV), which lacks GP64, utilizes LD130 as its envelope fusion protein. Homologs of ld130 have since been found not only in all the sequenced gp64-minus virus genomes, but also in the genomes of gp64-containing viruses. In addition, they are evolutionarily related to the envelope proteins of certain insect retroviruses. In this report, the characterization of a LD130 homolog (OP21) from OpMNPV, which also contains gp64, is described. Western blot analysis of extracts of OpMNPV-infected Lymantria dispar cells, using antibodies generated against OP21, identified an infected cell-specific doublet of 85 and 89 kDa. These bands were first observed at about 6 h p.i. and were present at all later time points. Such analyses also demonstrated that OP21 was associated with budded virions. Tunicamycin treatment of OpMNPV-infected cells indicated that OP21 is N-glycosylated. Studies employing NP-40 to remove the envelope from budded virions indicated that the majority of OP21 remained associated with the nucleocapsid fraction, whereas all GP64 was removed. Confocal immunofluorescence microscopy showed that OP21 and GP64 have a similar pattern of distribution on the membrane of cells infected with OpMNPV. Immunoelectron microscopy of budded virions also showed similar patterns of localization for both OP21 and GP64.

Protein disulfide isomerase in Alzheimer disease.

There is a great deal of evidence that places oxidative stress as a proximal event in the natural history of Alzheimer disease (AD). In addition to increased damage, there are compensatory increases in the levels of free sulfhydryls, glucose-6-phosphate dehydrogenase, and NAD(P)H:quinone oxidoreductase 1. To investigate redox homeostasis further in AD, we analyzed protein disulfide isomerase (PDI), a multifunctional enzyme, which catalyzes the disruption and formation of disulfide bonds. PDI plays a pivotal role in both secreted and cell-surface-associated protein disulfide rearrangement. In this study, we show that PDI specifically localizes to neurons, where there is no substantial increase in AD compared to age-matched controls. These findings indicate that the neurons at risk of death in AD do not show a substantial change in PDI to compensate for the increased sulfhydryls and reductive state found during the disease. This suggests that, despite compensatory reductive changes in AD, the level of PDI is sufficiently high physiologically in neurons to accommodate a more reducing environment.

Prostaglandin A1 inhibits stress-induced NF-kappaB activation and reverses resistance to topoisomerase II inhibitors.

Stress conditions associated with solid tumors lead to the formation of heterogeneous tumor cell subpopulations and insensitivity to cancer chemotherapeutics. In this report, we show that EMT6 mouse mammary tumor cells treated with the chemical stress, brefeldin A (BFA), or the physiological stress, hypoxia, develop resistance to the topoisomerase II (topoII) inhibitors teniposide and etoposide. BFA and hypoxia treatment did not alter intracellular drug concentrations, topoll protein levels, or inhibit topoII activity. BFA and hypoxia did cause the activation of the nuclear transcription factor NF-kappaB. We demonstrate that pretreatment with the synthetic cyclopentenone prostaglandin A1 (PGA1) inhibits stress-induced NF-kappaB activation and reverses BFA- and hypoxia-induced resistance. The reversal of BFA-induced resistance can occur when PGA1 is administered either before or several hours after the induction of stress. Taken together, these data support the involvement of NF-kappaB in stress-induced drug resistance, show that pharmacologic inhibitors of NF-kappaB can disrupt the biological consequences of stress, and imply that inhibitors of NF-kappaB may be useful agents to enhance the clinical efficacy of topoII-directed chemotherapeutics.

Increased neuronal glucose-6-phosphate dehydrogenase and sulfhydryl levels indicate reductive compensation to oxidative stress in Alzheimer disease.

We analyzed glucose-6-phosphate dehydrogenase, the rate-controlling enzyme of the pentose phosphate pathway and free sulfhydryls, to study redox balance in Alzheimer disease. Glucose-6-phosphate dehydrogenase plays a pivotal role in homeostatic redox control by providing reducing equivalents to glutathione, the major nonenzymatic cellular antioxidant. There is a multitude of evidence that marks oxidative stress proximally in the natural history of Alzheimer disease. Consistent with a role for glutathione in defense against increased reactive oxygen, we found an upregulation of glucose-6-phosphate dehydrogenase together with increased sulfhydryls in Alzheimer disease. These data indicate that reductive compensation may play an important role in combating oxidative stress in Alzheimer disease.

Using pork to teach students quality variations and how they are measured. 1998 UW-AS-305 Class.

Using a total of eight pork loins representing DFD (dark, firm, and dry) and PSE (pale, soft, and exudative) conditions, 35 students conducted a series of objective and subjective measurements to demonstrate extremes in meat quality in a single 2-h laboratory. Students learned to objectively assess appearance, water-holding and water-binding capacity, ultimate pH (pHu), and shear force (cooked samples) by operating seven commonly known laboratory instruments. They also learned how to prepare and present samples for organoleptic analysis using hedonic and triangle tests. Finally, the students learned the factors related to meat quality and how extremely they can vary. Within one laboratory, they observed that DFD, when compared with PSE, averaged 1.5 units higher in pHu, 4.7% (absolute) less drip loss, bound 136% (absolute) more water, was darker in color (26 units lower L* value), was firmer with a more attractive structure requiring 1 kg/cm less force to shear, and was superior in organoleptic properties (overall 21% more desirable). Having 35 replicates to use for the data set, the results illustrated statistically significant variations in meat-quality traits and how they could be objectively measured. Nine months later, 12 of the students were surveyed. It was their perception that the laboratory was not any more effective than other laboratories in the same class, but they were able to remember 85% of the methods used to measure quality; about twice that of other methods taught in other laboratory sessions.

beta-alanine and alpha-fluoro-beta-alanine concentrative transport in rat hepatocytes is mediated by GABA transporter GAT-2.

Studies on the compartmentalization of uridine catabolic metabolism in liver have indicated accumulation of beta-alanine as well as alpha-fluoro-beta-alanine (FbetaAL) for 5-fluorouracil in the hepatocytes. Using preparations of rat hepatocytes we were able to identify a Na+-dependent transport with high affinity for beta-alanine and GABA with Michaelis constant (Km) of 35.3 and 22.5 microM, respectively. A second Na+-dependent kinetic component with Km >1 mM was also identified. The sigmoidal profile of beta-alanine uptake with respect to Na+ shows the involvement of multiple ions of sodium in the transport process. A Hill coefficient of 2.6 +/- 0.4 indicates that at least two sodium ions are cotransported with beta-alanine. The flux of beta-alanine was also shown to be chlorine dependent. The substitution of this anion with gluconate, even in the presence of Na+, reduced the intracellular concentrative accumulation of beta-alanine to passive diffusion level, indicating that both Na+ and Cl- are essential for the activity of this transporter. The transport of beta-alanine was inhibited by GABA, hypotaurine, beta-aminoisobutyric acid, and FbetaAL in a competitive manner. However, concentrations up to 1 mM of L- and D-alanine, taurine, and alpha-aminoisobutyric acid did not affect beta-alanine uptake. Considering the similarities in substrate specificity with the rat GAT-2 transporter, extracts of hepatocytes were probed with the anti-GABA transporter antibody R-22. A 80-kDa band corresponding to GAT-2 was present in the hepatocyte and in the GAT-2 transfected Madin-Darby canine kidney cell extract, confirming the extraneural localization of this transporter. In view of these results, the neurotoxic effects related to the administration of uridine and 5-fluorouracil could be explained with the formation of beta-alanine and FbetaAL and their effect on the cellular reuptake of GABA.

Relationship of nm23 to proteolytic factors, proliferation and motility in breast cancer tissues and cell lines.

Low expression of the antimetastatic gene nm23 has been associated with shorter overall survival in breast cancer. To better understand the mechanism(s) of action of this protein, we compared the levels of the nm23 protein in 152 breast cancer samples with other factors known to be involved in metastasis or related to prognosis. There was no significant relationship between either of the nm23 isoforms and cathepsin D (Cat-D), urokinase plasminogen activator (uPA), its inhibitor (PAI-1), steroid hormone receptors or ploidy status. A marginal inverse correlation was observed between per cent S-phase and nm23-H1 expression (r = -0.193, P = 0.047) and a positive correlation was observed between uPA receptor (uPAR) and both nm23-H1 (r = 0.263, P = 0.0018) and nm23-H2 (r = 0.230, P = 0.0064). The nm23-H1 gene was transfected into MDA-MB-231 human breast cancer cells and 12 clones were selected, of which two were characterized extensively. We found no significant differences in Cat-D, uPA, PAI-1 or uPAR, as a function of nm23 expression in either the MDA-MB-231 cells or the transfected clones. Compared with the parent cell line, we did observe a dose-dependent decrease in growth factor-stimulated motility and a decrease in metastatic potential in two clones with four- and eightfold elevated nm23-H1 expression, whereas the proliferative activities were similar. We conclude that the decreased metastatic potential might be related to down-regulation of growth factor-stimulated motility.

Prevention of brefeldin A-induced resistance to teniposide by the proteasome inhibitor MG-132: involvement of NF-kappaB activation in drug resistance.

Brefeldin A, an agent that disrupts protein transport from the endoplasmic reticulum to the Golgi, induces the expression of GRP78 and the activation of nuclear factor (NF)-kappaB in cells. Treatment of cells with brefeldin A causes the development of resistance to topoisomerase II-directed agents, such as etoposide and doxorubicin. In this study, we show that treatment of EMT6 mouse mammary tumor cells with brefeldin A strongly induces GRP78 mRNA (8.5-fold) and resistance to teniposide (VM26). Treatment with okadaic acid causes a minor increase in GRP78 mRNA (2.1-fold) yet still induces resistance to VM26 as effectively as brefeldin A. In contrast, cells treated with castanospermine show a moderate increase in GRP78 mRNA (3.9-fold) but no resistance to VM26. These data imply that GRP78 induction does not mediate the development of drug resistance. An alternative mechanism of drug resistance may involve activation of the transcription factor, NF-kappaB, and we show that both brefeldin A and okadaic acid activate NF-kappaB in EMT6 cells. Furthermore, we demonstrate that treatment with the proteasome inhibitor MG-132 blocks the activation of NF-kappaB and prevents the development of resistance to VM26 induced by brefeldin A. Collectively, these results suggest that the resistance to VM26 in EMT6 cells treated with brefeldin A is mediated by the activation of NF-kappaB rather than the induction of GRP78. Our results also suggest that inhibition of NF-kappaB activation in tumor cells may increase the efficacy of topoisomerase II-directed agents in chemotherapy.

Linguistic psychotherapy research: new directions and promising findings.

Language configures experience and is our primary instrument of meaning making. Its central role in the construction of our subjective and interpersonal worlds provides the rationale for investigating its forms and functions in psychotherapy. Three clinically relevant dimensions of language (i.e., connectivity, modality, and complexity) are outlined and several examples of linguistic variables on each dimension are defined. Linguistic studies of psychotherapy are then presented in terms of focal points of assessment: pretherapy, intherapy, and posttherapy. At each focal point, innovative applications of linguistic variables are presented, often in contexts that permit direct contrast with more traditional methodologies. Promising preliminary results suggest that linguistic research can help to better differentiate and describe patient psychopathology at pretherapy, therapist and patient processes in therapy, and patient gains at posttherapy.

Psychiatric, neuropsychological, and psychosocial features of DSM-IV subtypes of attention-deficit/hyperactivity disorder: results from a clinically referred sample.

OBJECTIVE: To assess the validity of the DSM-IV subtypes of attention-deficit/hyperactivity disorder (ADHD). METHOD: Using structured diagnostic interviews and psychometric measures of cognitive and social functioning, the authors assessed 413 children and adolescents consecutively referred to a pediatric psychopharmacology clinic since 1991. RESULTS: Marked psychiatric differences were found among DSM-IV subtypes of ADHD, but few differences were found in cognitive or psychosocial functioning. The greatest psychiatric differences were found between the combined-type subjects (who tended to show more impairment in multiple domains) and the other two subgroups. The inattentive patients, however, were more likely to have required extra help in school. The hyperactive-impulsive patients were not different from controls on rates of depression, Child Behavior Checklist measures of social functioning, or psychometric measures of intellectual functioning and academic achievement. CONCLUSIONS: The results suggest that, regarding clinical features, combined-type patients have a more severe disorder than the other DSM-IV subtypes.

Can pale, soft, exudative pork be prevented by postmortem sodium bicarbonate injection?

Previous attempts at eliminating the problem of PSE pork by genetic selection or rapid postmortem cooling have been only partially successful. A new approach, namely, postmortem injection of sodium bicarbonate (SBC), was tested on halothane-positive gilts. Sixteen pigs were used to establish a suitable SBC concentration. At approximately 15 min after death, the longissimus of one side of the carcass was injected with 10% (by weight) of .2 to .4 M SBC solutions containing .7% NaCl (wt/vol). All concentrations resulted in a higher ultimate pH, improved muscle color, and reduced drip loss. In a second experiment, with 23 pigs, .3 M SBC was injected into the longissimus and the biceps femoris at either 15 min or 24 h after death and with or without inclusion of .7% NaCl (wt/vol). Compared with controls, the 15-min SBC + NaCl injected samples had darker color (L* of 47 vs 53 in controls), higher ultimate pH (5.6 vs 5.3), lower drip loss (5% vs 10%), and increased protein solubility (140 vs 115 mg/g). Injection at 24 h reduced drip loss (from 10% to 5.7%) but did not correct the color defect. The SBC alone and SBC + NaCl treatments had essentially the same effects in reducing drip loss, increasing ultimate pH, and improving color; but the SBC-NaCl injected samples had improved juiciness and flavor compared with SBC. Early postmortem sodium bicarbonate injection seems to prevent the development of PSE pork when injected into carcasses of halothane-sensitive pigs.

Correspondence between DSM-III-R and DSM-IV attention-deficit/hyperactivity disorder.

OBJECTIVE: To evaluate the correspondence between DSM-III-R and DSM-IV definitions of attention-deficit/hyperactivity disorder (ADHD) in clinically referred children. Results of the field trials led to the hypothesis that there would be a strong correspondence between DSM-III-R and DSM-IV subtypes. METHOD: The sample consisted of all children and adolescents consecutively referred to a pediatric psychopharmacology clinic (N = 405). Children were comprehensively evaluated with structured diagnostic interviews assessing both DSM-III-R and DSM-IV ADHD. DSM-III-R symptoms were used to approximate DSM-IV subtypes. Kappa statistics and conditional probabilities were used to examine the correspondence between DSM-III-R and DSM-IV ADHD. RESULTS: Ninety-three percent of children who received a DSM-III-R diagnosis of ADHD also received a DSM-IV ADHD diagnosis. The kappa coefficient assessing the agreement between DSM-III-R and DSM-IV ADHD was .73 (z = 14.6, p < .0001). The kappa coefficient assessing the agreement between the DSM-III-R-approximated subtypes and the actual DSM-IV subtypes was .71 (z = 15, p < .0001). CONCLUSION: These results confirm previous findings and indicate that the change from DSM-III-R to DSM-IV results in minimal changes in case identification and provides support for diagnostic continuity between the two classification systems.

Characterization of P91, a protein associated with virions of an Orgyia pseudotsugata baculovirus.

Polyclonal antiserum produced against preoccluded virions from the Orgyia pseudotsugata multinucleocapsid nuclear polyhedrosis virus (OpMNPV) was used to screen an OpMNPV lambda gt11 expression library. The insert from one of the immunoreactive phage isolates hybridized to OpMNPV orf86 (p91), a 2460-bp (819 amino acids) open reading frame that encodes a predicted protein of 91 kDa. Antibodies generated against a maltose binding protein-P91 fusion detected a band of approximately 91 kDa on Western blots of extracts of OpMNPV-infected Lymantria dispar cells. This band was first observed at 18 hr p.i. and was present at all later time points. Similar results using this antiserum were seen with a time course of Autographa californica-infected Spodoptera frugiperda cells. Localization of P91 by confocal immunofluorescence microscopy showed that the protein was concentrated near the nuclear membrane and at late times p.i. was most concentrated near polyhedra. Immunoelectron microscopy indicated that P91 was present in both the capsid and envelope surrounding the capsid of occlusion-derived virions. Fractionation studies employing NP-40 and Western blot analysis indicated that P91 was associated with the capsid structure.

nm23--relationship to the metastatic potential of breast carcinoma cell lines, primary human xenografts, and lymph node negative breast carcinoma patients.

BACKGROUND: Since the discovery of nm23 (nonmetastatic) by Steeg et al. in 1988, a number of tumor cohort studies have shown an inverse relationship between the levels of expression of the nm23-H1 protein and disease aggressiveness and tumor metastatic potential. METHODS: The relationship between the expression of nm23 protein and the metastatic potential of human breast carcinoma was analyzed in cell lines, xenografts, and in a retrospective lymph node negative breast carcinoma population. The lymph node negative breast carcinoma study was comprised of 40 patients: 19 with nonrecurrent and 21 with recurrent disease. The 40 patients were matched according to age, cathepsin D, tumor size, percent S-phase, DNA ploidy, steroid receptor status, and tumor grade. Nm23-H1 protein levels in cell lines and xenografts were analyzed quantitatively using Western blot analyses and semiquantitatively in tissue sections using immunocytochemistry. Immunocytochemical analysis of lymph node negative breast tumors was graded as the percent of tumor staining positive for nm23 and the intensity of staining. The metastatic potentials of the cell lines and xenografts were assessed as the ability to form metastatic lesions in nude mice. In the lymph node negative breast carcinoma patients, the metastatic potential was characterized as the incidence of breast carcinoma recurrence. RESULTS: The MCF-7 cell line expressed four- and tenfold higher levels of nm23-H1 than the highly metastatic MDA-MB-435 and MDA-MB-231 cells, respectively. Among the xenografts and cell lines, there was an inverse correlation between nm23-H1 expression and metastatic potential in athymic nude mice (correlation coefficient [R] = -0.51). The differences between the levels of nm23-H1 among the metastatic and nonmetastatic cell lines and xenografts were not statistically significant. Statistical analyses indicated that neither the intensity nor the percent of tumor staining positive for nm23 expression was correlated to the recurrence of breast carcinoma in the lymph node negative patient population that had been matched for other clinical prognostic markers. CONCLUSIONS: There was an inverse correlation (R = 0.51) between the levels of nm23-H1 expression in cell lines and xenografts and the metastatic potential in nude mice. In the retrospective lymph node negative breast carcinoma population, no clear association was demonstrated between the expression of nm23 and breast carcinoma recurrence. This observation suggests the nm23 expression does not predict outcome in lymph node negative breast carcinoma patients.