Comparison of independent and traditional registered nurse learners in a physical assessment course.

The purpose of this study was to determine if there was a significant difference in the time used to complete a neurological assessment by students who studied physical assessment and practiced independently when compared to students who used the traditional lecture method of instruction and practiced with the instructor. The research methodology utilized a descriptive comparative design. The convenience sample consisted of 20 Registered Nurses (RNs) randomly selected from a class of 34 RN students in one section of an undergraduate Physical Assessment course. A watch was used to measure the time the student used to complete the neurological assessment. A one-tailed independent samples t-test was used to compare the difference in time used as indicated by the means of the two groups. The level of significance was 0.05. The result of the study is that there was no significant difference found between the two groups on the amount of time used to complete a neurological assessment p > .05, t = 1.151, p = .303. The conclusion of this study was that RN students are able to learn physical assessment independently and successfully complete a neurological assessment in a similar amount of time as RN students who use the traditional classroom method. Recommendations include replicating the study with a larger sample and with students in a Graduate Health Assessment course to determine if similar results will occur.

Nephritogenic T cells use granzyme C as a cytotoxic mediator.

Cytoplasmic granules of cytotoxic T lymphocytes contain several proteins that may be involved in cell-mediated cytotoxicity. We have previously described nephritogenic T cell clones that are cytotoxic to cultured renal proximal tubular epithelial cells (MCT). One of these clones, M52.34.1, expresses perforin, a cytotoxic mediator. We investigated the expression of other granule-associated proteases of M52.34.1. Granzymes A and B have been extensively studied in T cell-mediated cytotoxicity, and associated with tissue destruction in models of transplantation. However, the activity of other granzymes has not been as extensively investigated. We focused our studies on granzyme C. Northern blots showed very high levels of granzymes B and C mRNA expression in M52.34.1 cells 3 days following T cell activation. There was no expression of granzyme A mRNA. An antisense oligonucleotide made from the 5'-upstream region of the murine granzyme C exon 1 inhibited granzyme C mRNA expression in M52.34.1 when added at a concentration of 50 microM to the culture medium for 2 days. There was no inhibition of granzyme C mRNA expression with the sense oligonucleotide. The granzyme C antisense oligonucleotide inhibited M52.34.1 cytotoxicity to MCT at effector:target ratios of 20:1 and 40:1. M52.34.1 cells mediate inflammatory interstitial nephritis following adoptive transfer. If T cells were resuspended in 200 microM of the antisense oligonucleotide prior to subcapsular transfer, the recipient kidneys showed markedly diminished tubular cell destruction, suggesting that granzyme C can also be an important mediator of cytotoxicity in vivo.

Loss of high affinity transforming growth factor-beta 1 (TGF-beta 1) binding to a nephritogenic T cell results in absence of growth inhibition by TGF-beta 1 and augmented nephritogenicity.

Transforming growth factor-beta (TGF-beta) affects cellular proliferation and differentiation and has been linked to the development of pathologic extracellular matrix production characteristic of progressive renal disease. TGF-beta 1 is conventionally regarded as having growth-inhibitory activity on T lymphocytes. The growth-regulatory activity of TGF-beta 1 depends on the interaction of TGF-beta 1 with its receptors, especially the type I and II receptors. In this study, we describe a CD4+ nephritogenic T cell clone that, unlike a sister clone with an identical TCR Ag receptor, is not growth inhibited by TGF-beta 1, nor is its nephritogenicity affected by exogenous TGF-beta 1. Although this TGF-beta-resistant T cell clone expresses both type I and II TGF-beta receptors on the cell surface, the affinity of this interaction is markedly diminished compared with that of the sister T cell clone, which does undergo growth arrest in response to extracellular TGF-beta 1. The resistant T cell clone expresses one mutant allele for the type I TGF-beta receptor. This mutation consists of a leucine to glutamine substitution at codon 122, a conserved amino acid in the transmembrane domain. We speculate that this mutation alters the interaction between the type I and II TGF-beta receptors following recognition of ligand by the type II receptor.

Cluster care: an alternative to traditional care.

Studies of client satisfaction of the Traditional and Cluster Care service delivery models are virtually nonexistent. In an effort to provide healthcare services to Medicaid-eligible elderly home care clients, the New York City Human Resources Administration has implemented a new concept, Cluster Care. Because Cluster Care is probably going to be the wave of the 21st century, nurses need to be creative so that this new model will be more palatable to its recipients.

Complexity of the immunoglobulin light chain V kappa 1 gene family in the New Zealand black mouse.

The immunoglobulin light chain V kappa 1 gene family is polymorphic in murine inbred strains and this family has been subdivided into five sub-groups (V kappa 1A-E). The V kappa 1A sub-group contributes to approximately 2% of the total serum immunoglobulin light chains in several mouse strains. However, it has been reported that this sub-group is absent in New Zealand Black (NZB) mouse serum. Amino acid sequencing of myeloma proteins from this inbred mouse has shown that they belong to the V kappa 1B sub-group. We report here the structure of nine functional germline genes from NZB mice that have high homologies to the V kappa 1A, V kappa 1B, V kappa 1C, and V kappa 1D sub-groups. In addition, a novel germline gene representing the prototype of a new sub-group (designated V kappa 1F) has been identified. We have isolated different V kappa 1 germline genes from a single restriction fragment length polymorphism (RFLP) fragment, as well as identical V genes from two different RFLP migrating bands. Therefore, the complexity of the genes encoding the immunoglobulin variable region cannot be determined solely by RFLP analysis. Nucleotide sequence analysis of 16 V kappa 1 genes which code for NZB autoantibodies indicate that they belong to five different V kappa 1 sub-groups with five hybridomas (31%) expressing the V kappa 1A sub-group. Comparison of the sequences of V kappa 1 genes expressed in hybridomas with corresponding germline genes show no somatic mutations.

Correlation between the occurrence of lupus nephritis, anti-erythrocyte autoantibodies and V kappa haplotype in NZB x 129/J and NZB x SM/J recombinant inbred murine strains.

The NZB mouse is genetically predisposed to the development of autoimmune disease that resembles the human autoimmune systemic lupus erythematosus and autoimmune hemolytic anemia, with increased titers of anti-DNA, and Coombs' autoantibodies. The various autoimmune traits are controlled separately by a limited number of genes. Genetic studies have shown that several immune loci are involved in autoimmunity: T cell abnormalities, H-2 complex and immunoglobulin genes have been implicated. In this report, we present evidence for a significant correlation of NZB V kappa 1 haplotype defined by restriction fragment length polymorphism analysis with anti-erythrocyte autoantibodies in NZB x 129/J and NZB x SM/J recombinant inbred lines.

Mental health benefits: breaking through the clouds.

One state after another is making sure you can't simply cut or drop mental health benefits. But some creative companies are turning a liability into an asset.

Activation of clones producing self-reactive antibodies by foreign antigen and antiidiotype antibody carrying the internal image of the antigen.

Because we found in previous work that a high fraction of antibodies exhibiting various specificities bound to glutamic acid 50-tyrosine50 homopolymer (GT) and expressed pGAT cross-reactive idiotype (IdX), we studied the activation of clones producing multireactive antibodies in 1-mo-old MRL/lpr and C3H/HeJ mice bearing VHJ haplotype. The activation of such clones was studied after mice were immunized with GT in CFA, HP20 (an anti-Id MAb carrying the internal image of GT in the D region), and a synthetic peptide corresponding to the D segment of HP20. Our results indicate that immunized mice produced both GT- and self-reactive antibodies. Study of the immunochemical properties of MAb showed that they exhibit multispecific properties and bind with similar-affinity constants to GT or self-antigens such as DNA, Smith antigen (Sm), and IgG2a. An important fraction of antibodies obtained from MRL/lpr mice immunized with HP20 expressed pGAT IdX and some of these antibodies share IdX expressed on anti-DNA, Sm, and rheumatoid factor (RFs) antibodies. The hybridomas producing multispecific autoantibodies use heavy-chain- (VH) and light-chain-variable region (VK) genes from various V gene families, suggesting that they do not derive from the pool of GAT precursors. Sequencing of VH and VK genes of two antibodies show that they can use closely related VHJ558, unmutated VK1, or different VK genes than those used by anti-GT antibodies. Our data demonstrate that clones producing antibodies binding to GT and self-antigens with similar-affinity constants can be activated by foreign or anti-Id antibodies carrying the internal image of the antigen or even by a synthetic peptide corresponding to the D segment of anti-Id antibodies.

Fatty acid-binding protein: a major contributor to the ethanol-induced increase in liver cytosolic proteins in the rat.

To study the acute and chronic effects of ethanol on hepatic fatty acid-binding protein, rats were pair-fed with liquid diets containing 36% of energy either as ethanol or as additional carbohydrate for 4 to 5 weeks. Animals were killed 90 min after intragastric administration of diets with or without ethanol. Alcohol feeding markedly increased liver triglycerides, with a modest rise in nonesterified fatty acids. Alcohol-fed rats developed hepatomegaly, with a 48% increase in hepatic cytosolic proteins. Fatty acid binding was first assessed by the kinetics of [14C]palmitate binding to cytosolic proteins. The maximal binding capacity more than doubled in the cytosol of the ethanol-fed rats compared to pair-fed controls, whereas the dissociation constant increased by 64%. Acute ethanol administration (3 gm per kg body weight) either to ethanol-fed or control rats did not have a significant effect. To identify the fatty acid-binding protein, labeled cytosolic proteins were fractionated by gel filtration: most of the cytosolic fatty acids eluted as a single peak in the 12,000 to 18,000 molecular weight region corresponding to the hepatic fatty acid-binding protein. The increase in this protein, confirmed by radial immunodiffusion (27.0 +/- 1.4 mg per 100 gm body weight vs. 11.2 +/- 1.6, in controls; p less than 0.01), accounted for 22% of the total rise in cytosolic protein induced by chronic ethanol feeding.