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1.
Br J Pharmacol ; 157(7): 1263-9, 2009 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-19563529

RESUMO

BACKGROUND AND PURPOSE: Previous results have shown that mice lacking in the group 1B phospholipase A(2) (Pla2g1b) are resistant to obesity and diabetes induced by feeding a diabetogenic high-fat/high-carbohydrate diet. This study examined the potential of using the Pla2g1b inhibitor methyl indoxam as therapy to suppress diet-induced obesity and diabetes. EXPERIMENTAL APPROACH: Male C57BL/6 mice were fed the diabetogenic diet with or without methyl indoxam supplementation. Body weight gain, fasting plasma glucose levels, glucose tolerance and postprandial lysophospholipid absorption were compared. KEY RESULTS: Wild-type C57BL/6 mice fed the diabetogenic diet without Pla2g1b inhibitor showed 31 and 69% body weight gain after 4 and 10 weeks respectively. These animals also showed elevated plasma glucose levels and were glucose intolerant. In contrast, C57BL/6 mice fed the diabetogenic diet with 90 mg.kg(-1) of methyl indoxam gained only 5% body weight after 10 weeks. These animals were also euglycaemic and displayed normal glucose excursion rates in glucose tolerance test. Methyl indoxam suppression of diet-induced body weight gain and glucose intolerance was correlated with the inhibition of Pla2g1b-mediated postprandial lysophospholipid absorption. CONCLUSIONS AND IMPLICATIONS: These results show that oral supplementation of a diabetogenic diet with the Pla2g1b inhibitor methyl indoxam effectively suppresses diet-induced obesity and diabetes in mice. This suggests that Pla2g1b inhibition may be a potentially effective oral therapeutic option for treatment of obesity and diabetes.


Assuntos
Fármacos Antiobesidade/uso terapêutico , Compostos de Bifenilo/farmacologia , Intolerância à Glucose/tratamento farmacológico , Fosfolipases A2 do Grupo IB/antagonistas & inibidores , Hipoglicemiantes/uso terapêutico , Indóis/farmacologia , Obesidade/tratamento farmacológico , Animais , Fármacos Antiobesidade/farmacocinética , Bile/efeitos dos fármacos , Bile/enzimologia , Células CACO-2 , Carboidratos da Dieta/administração & dosagem , Gorduras na Dieta/administração & dosagem , Ingestão de Alimentos/efeitos dos fármacos , Intolerância à Glucose/sangue , Intolerância à Glucose/etiologia , Fosfolipases A2 do Grupo IB/genética , Fosfolipases A2 do Grupo IB/metabolismo , Humanos , Hidrólise , Hipoglicemiantes/farmacocinética , Lisofosfolipídeos/sangue , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Obesidade/sangue , Obesidade/etiologia , Período Pós-Prandial , Proteínas Recombinantes/antagonistas & inibidores , Proteínas Recombinantes/metabolismo , Aumento de Peso/efeitos dos fármacos
2.
Mol Biol Cell ; 12(11): 3668-79, 2001 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-11694597

RESUMO

The yeast actin-regulating kinases Ark1p and Prk1p are signaling proteins localized to cortical actin patches, which may be sites of endocytosis. Interactions between the endocytic proteins Pan1p and End3p may be regulated by Prk1p-dependent threonine phosphorylation of Pan1p within the consensus sequence [L/I]xxQxTG. We identified two Prk1p phosphorylation sites within the Pan1p-binding protein Ent1p, a yeast epsin homologue, and demonstrate Prk1p-dependent phosphorylation of both threonines. Converting both threonines to either glutamate or alanine mimics constitutively phosphorylated or dephosphorylated Ent1p, respectively. Synthetic growth defects were observed in a pan1-20 ENT1(EE) double mutant, suggesting that Ent1p phosphorylation negatively regulates the formation/activity of a Pan1p-Ent1p complex. Interestingly, pan1-20 ent2 Delta but not pan1-20 ent1 Delta double mutants had improved growth and endocytosis over the pan1-20 mutant. We found that actin-regulating Ser/Thr kinase (ARK) mutants exhibit endocytic defects and that overexpressing either wild-type or alanine-substituted Ent1p partially suppressed phenotypes associated with loss of ARK kinases, including growth, endocytosis, and actin localization defects. Consistent with synthetic growth defects of pan1-20 ENT1(EE) cells, overexpressing glutamate-substituted Ent1p was deleterious to ARK mutants. Surprisingly, overexpressing the related Ent2p protein could not suppress ARK kinase mutant phenotypes. These results suggest that Ent1p and Ent2p are not completely redundant and may perform opposing functions in endocytosis. These data support the model that, as for clathrin-dependent recycling of synaptic vesicles, yeast endocytic protein phosphorylation inhibits endocytic functions.


Assuntos
Proteínas Adaptadoras de Transdução de Sinal , Proteínas de Transporte/metabolismo , Endocitose/fisiologia , Proteínas Fúngicas , Proteínas Serina-Treonina Quinases/metabolismo , Receptores Proteína Tirosina Quinases/metabolismo , Proteínas de Saccharomyces cerevisiae , Proteínas de Transporte Vesicular , Actinas/metabolismo , Proteínas Adaptadoras de Transporte Vesicular , Sítios de Ligação , Proteínas de Transporte/genética , Sequência Consenso , Citoesqueleto/metabolismo , Proteínas de Fluorescência Verde , Proteínas Luminescentes/genética , Proteínas Luminescentes/metabolismo , Neuropeptídeos/metabolismo , Fosforilação , Proteína Quinase C , Proteínas Serina-Treonina Quinases/genética , Proteínas Serina-Treonina Quinases/fisiologia , Receptores Proteína Tirosina Quinases/genética , Receptores Proteína Tirosina Quinases/fisiologia , Proteínas Recombinantes de Fusão/genética , Proteínas Recombinantes de Fusão/metabolismo , Saccharomyces cerevisiae/efeitos dos fármacos , Saccharomyces cerevisiae/enzimologia , Saccharomyces cerevisiae/genética , Saccharomyces cerevisiae/crescimento & desenvolvimento , Sorbitol/farmacologia , Temperatura , Treonina/metabolismo
3.
Nat Cell Biol ; 3(7): 687-90, 2001 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-11433303

RESUMO

Longstanding evidence supports a role for actin in endocytosis; an intact actin cytoskeleton is required for endocytosis in yeast, and drugs that inhibit actin polymerization inhibit endocytosis in both yeast and mammalian cells. The yeast Arp2/3 complex is required for the internalization step of endocytosis. In addition, some early endocytic events in mammalian cells are associated with the formation of actin tails similar to those generated by activated Arp2/3 complex. However, until now no Arp2/3 complex activator has been identified among proteins known to mediate early steps in endocytosis. Here we show that the yeast endocytic protein Pan1p binds to and activates the Arp2/3 complex. Genetic interactions between PAN1 and mutants of Arp2/3 subunits, or of the Arp2/3 activator LAS17, provide evidence for this activity in vivo. We suggest that Pan1p forms the core of an endocytic complex and physically couples actin polymerization nucleated by the Arp2/3 complex to the endocytic machinery, thus providing the forces necessary for endocytosis.


Assuntos
Actinas/efeitos dos fármacos , Proteínas de Ligação ao Cálcio/fisiologia , Proteínas do Citoesqueleto , Proteínas Fúngicas/farmacologia , Fosfoproteínas/fisiologia , Saccharomyces/química , Proteína 2 Relacionada a Actina , Proteína 3 Relacionada a Actina , Actinas/metabolismo , Sequência de Aminoácidos , Relação Dose-Resposta a Droga , Endocitose/efeitos dos fármacos , Proteínas Fúngicas/genética , Cinética , Proteínas dos Microfilamentos , Ligação Proteica , Proteínas de Saccharomyces cerevisiae , Alinhamento de Sequência , Deleção de Sequência
4.
Plant Physiol ; 125(1): 360-8, 2001 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-11154343

RESUMO

We have previously shown that the wheat (Triticum aestivum) TaADF gene expression level is correlated with the plants capacity to tolerate freezing. Sequence analysis revealed that this gene encodes a protein homologous to members of the actin-depolymerizing factor (ADF)/cofilin family. We report here on the characterization of the recombinant TaADF protein. Assays for ADF activity showed that TaADF is capable of sequestering actin, preventing nucleotide exchange, and inducing actin depolymerization. In vitro phosphorylation studies showed that TaADF is a substrate for a wheat 52-kD kinase. The activity of this kinase is modulated by low temperature during the acclimation period. Western-blot analyses revealed that TaADF is expressed only in cold-acclimated Gramineae species and that the accumulation level is much higher in the freezing-tolerant wheat cultivars compared with the less tolerant ones. This accumulation was found to be regulated by a factor(s) encoded by a gene(s) located on chromosome 5A, the chromosome most often found to be associated with cold hardiness. The induction of an active ADF during cold acclimation and the correlation with an increased freezing tolerance suggest that the protein may be required for the cytoskeletal rearrangements that may occur upon low temperature exposure. These remodelings might be important for the enhancement of freezing tolerance.


Assuntos
Aclimatação/fisiologia , Proteínas dos Microfilamentos/genética , Proteínas de Plantas/genética , Triticum/fisiologia , Fatores de Despolimerização de Actina , Sequência de Aminoácidos , Clonagem Molecular , Temperatura Baixa , Destrina , Regulação Enzimológica da Expressão Gênica , Regulação da Expressão Gênica de Plantas , Proteínas dos Microfilamentos/química , Proteínas dos Microfilamentos/metabolismo , Dados de Sequência Molecular , Fosforilação , Proteínas de Plantas/química , Proteínas de Plantas/metabolismo , Proteínas Quinases/metabolismo , Proteínas Recombinantes/química , Proteínas Recombinantes/metabolismo , Alinhamento de Sequência , Homologia de Sequência de Aminoácidos , Triticum/genética
6.
Mol Biol Cell ; 10(7): 2265-83, 1999 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-10397764

RESUMO

Sla2p, also known as End4p and Mop2p, is the founding member of a widely conserved family of actin-binding proteins, a distinguishing feature of which is a C-terminal region homologous to the C terminus of talin. These proteins may function in actin cytoskeleton-mediated plasma membrane remodeling. A human homologue of Sla2p binds to huntingtin, the protein whose mutation results in Huntington's disease. Here we establish by immunolocalization that Sla2p is a component of the yeast cortical actin cytoskeleton. Deletion analysis showed that Sla2p contains two separable regions, which can mediate association with the cortical actin cytoskeleton, and which can provide Sla2p function. One localization signal is actin based, whereas the other signal is independent of filamentous actin. Biochemical analysis showed that Sla2p exists as a dimer in vivo. Two-hybrid analysis revealed two intramolecular interactions mediated by coiled-coil domains. One of these interactions appears to underlie dimer formation. The other appears to contribute to the regulation of Sla2p distribution between the cytoplasm and plasma membrane. The data presented are used to develop a model for Sla2p regulation and interactions.


Assuntos
Actinas/metabolismo , Proteínas de Transporte/metabolismo , Citoesqueleto/metabolismo , Proteínas Fúngicas/metabolismo , Proteínas de Saccharomyces cerevisiae , Actinas/ultraestrutura , Sequência de Bases , Proteínas de Transporte/genética , Proteínas de Transporte/imunologia , Divisão Celular/genética , Proteínas do Citoesqueleto , Proteínas de Ligação a DNA/metabolismo , Dimerização , Endocitose , Proteínas Fúngicas/genética , Proteínas Fúngicas/imunologia , Deleção de Genes , Dados de Sequência Molecular , Mutação , Proteínas Recombinantes/genética , Proteínas Recombinantes/metabolismo , Transdução de Sinais , Leveduras/genética , Leveduras/metabolismo
7.
J Cell Biol ; 144(6): 1203-18, 1999 Mar 22.
Artigo em Inglês | MEDLINE | ID: mdl-10087264

RESUMO

Ark1p (actin regulating kinase 1) was identified as a yeast protein that binds to Sla2p, an evolutionarily conserved cortical actin cytoskeleton protein. Ark1p and a second yeast protein, Prk1p, contain NH2-terminal kinase domains that are 70% identical. Together with six other putative kinases from a number of organisms, these proteins define a new protein kinase family that we have named the Ark family. Lack of both Ark1p and Prk1p resulted in the formation of large cytoplasmic actin clumps and severe defects in cell growth. These defects were rescued by wild-type, but not by kinase-dead versions of the proteins. Elevated levels of either Ark1p or Prk1p caused a number of actin and cell morphological defects that were not observed when the kinase-dead versions were overexpressed instead. Ark1p and Prk1p were shown to localize to actin cortical patches, making these two kinases the first signaling proteins demonstrated to be patch components. These results suggest that Ark1p and Prk1p may be downstream effectors of signaling pathways that control actin patch organization and function. Furthermore, results of double-mutant analyses suggest that Ark1p and Prk1p function in overlapping but distinct pathways that regulate the cortical actin cytoskeleton.


Assuntos
Actinas/metabolismo , Proteínas Serina-Treonina Quinases/metabolismo , Receptores Proteína Tirosina Quinases/metabolismo , Proteínas de Saccharomyces cerevisiae , Saccharomyces cerevisiae/metabolismo , Sequência de Aminoácidos , Aurora Quinases , Sequência de Bases , Citoesqueleto/metabolismo , Primers do DNA/genética , Proteínas Fúngicas/metabolismo , Deleção de Genes , Genes Fúngicos , Dados de Sequência Molecular , Fenótipo , Proteína Quinase C , Proteínas Serina-Treonina Quinases/genética , Receptores Proteína Tirosina Quinases/genética , Saccharomyces cerevisiae/citologia , Saccharomyces cerevisiae/genética , Homologia de Sequência de Aminoácidos , Temperatura
8.
Mol Biol Cell ; 10(3): 581-96, 1999 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-10069805

RESUMO

Recent cloning of a rat brain phosphatidylinositol 3,4, 5-trisphosphate binding protein, centaurin alpha, identified a novel gene family based on homology to an amino-terminal zinc-binding domain. In Saccharomyces cerevisiae, the protein with the highest homology to centaurin alpha is Gcs1p, the product of the GCS1 gene. GCS1 was originally identified as a gene conditionally required for the reentry of cells into the cell cycle after stationary phase growth. Gcs1p was previously characterized as a guanosine triphosphatase-activating protein for the small guanosine triphosphatase Arf1, and gcs1 mutants displayed vesicle-trafficking defects. Here, we have shown that similar to centaurin alpha, recombinant Gcs1p bound phosphoinositide-based affinity resins with high affinity and specificity. A novel GCS1 disruption strain (gcs1Delta) exhibited morphological defects, as well as mislocalization of cortical actin patches. gcs1Delta was hypersensitive to the actin monomer-sequestering drug, latrunculin-B. Synthetic lethality was observed between null alleles of GCS1 and SLA2, the gene encoding a protein involved in stabilization of the actin cytoskeleton. In addition, synthetic growth defects were observed between null alleles of GCS1 and SAC6, the gene encoding the yeast fimbrin homologue. Recombinant Gcs1p bound to actin filaments, stimulated actin polymerization, and inhibited actin depolymerization in vitro. These data provide in vivo and in vitro evidence that Gcs1p interacts directly with the actin cytoskeleton in S. cerevisiae.


Assuntos
Actinas/metabolismo , Actinas/ultraestrutura , Proteínas de Ligação a DNA/metabolismo , Proteínas Fúngicas/metabolismo , Proteínas de Ligação ao GTP/metabolismo , Proteínas Ativadoras de GTPase , Proteínas dos Microfilamentos , Proteínas de Saccharomyces cerevisiae , Saccharomyces cerevisiae/metabolismo , Fator 1 de Ribosilação do ADP , Fatores de Ribosilação do ADP , Sequência de Aminoácidos , Animais , Sítios de Ligação , Proteínas de Transporte/genética , Proteínas de Transporte/metabolismo , Proteínas do Citoesqueleto/metabolismo , Citoesqueleto/metabolismo , Citoesqueleto/ultraestrutura , Proteínas de Ligação a DNA/genética , Proteínas Fúngicas/genética , Deleção de Genes , Glicoproteínas de Membrana/genética , Glicoproteínas de Membrana/metabolismo , Dados de Sequência Molecular , Mutação , Fosfatidilinositóis/metabolismo , Ratos , Saccharomyces cerevisiae/citologia , Saccharomyces cerevisiae/genética , Homologia de Sequência de Aminoácidos , Zinco/metabolismo , Dedos de Zinco
10.
Genetics ; 148(4): 1951-61, 1998 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-9560408

RESUMO

The mouse dilute (d) locus encodes unconventional myosin-VA (MyoVA). Mice carrying null alleles of dilute have a lightened coat color and die from a neurological disorder resembling ataxia and opisthotonus within three weeks of birth. Immunological and ultrastructural studies suggest that MyoVA is involved in the transport of melanosomes in melanocytes and smooth endoplasmic reticulum in cerebellar Purkinje cells. In studies described here, we have used an RT-PCR-based sequencing approach to identify the mutations responsible for 17 viable dilute alleles that vary in their effects on coat color and the nervous system. Seven of these mutations mapped to the MyoVA motor domain and are reported here. Crystallographic modeling and mutant expression studies were used to predict how these mutations might affect motor domain function and to attempt to correlate these effects with the mutant phenotype.


Assuntos
Proteínas de Filamentos Intermediários/genética , Mutagênese , Cadeias Pesadas de Miosina , Miosina Tipo V , Alelos , Animais , Cristalografia por Raios X , Feminino , Expressão Gênica , Cor de Cabelo/genética , Proteínas de Filamentos Intermediários/química , Masculino , Camundongos , Modelos Moleculares
11.
Nat Genet ; 16(2): 188-90, 1997 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-9171832

RESUMO

Genetic hearing impairment affects around 1 in every 2,000 births. The bulk (approximately 70%) of genetic deafness is non-syndromic, in which hearing impairment is not associated with any other abnormalities. Over 25 loci involved in non-syndromic deafness have been mapped and mutations in connexin 26 have been identified as a cause of non-sydromic deafness. One locus for non-syndromic recessive deafness, DFNB2 (ref. 4), has been localized to the same chromosomal region, 11q14, as one of the loci, USH1B, underlying the recessive deaf-blind syndrome. Usher syndrome type 1b, which is characterized by profound congenital sensorineural deafness, constant vestibular dysfunction and prepubertal onset of retinitis pigmentosa. Recently, it has been shown that a gene encoding an unconventional myosin, myosin VIIA, underlies the mouse recessive deafness mutation, shaker-1 (ref. 5) as well as Usher syndrome type 1b. Mice with shaker-1 demonstrate typical neuroepithelial defects manifested by hearing loss and vestibular dysfunction but no retinal pathology. Differences in retinal patterns of expression may account for the variance in phenotype between shaker-1 mice and Usher type 1 syndrome. Nevertheless, the expression of MYO7A in the neuroepithelium suggests that it should be considered a candidate for non-syndromic deafness in the human population. By screening families with non-syndromic deafness from China, we have identified two families carrying MYO7A mutations.


Assuntos
Surdez/genética , Genes Recessivos , Mutação , Miosinas/genética , Adulto , Animais , Cromossomos Humanos Par 11 , Dineínas , Éxons , Heterozigoto , Humanos , Camundongos , Pessoa de Meia-Idade , Miosina VIIa , Linhagem , Splicing de RNA
12.
Genes Funct ; 1(3): 191-203, 1997 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-9680294

RESUMO

The shaker-1 (Myo7a) mouse deafness locus is encoded by an unconventional myosin gene: myosin VIIA [Gibson, Walsh, Mburu, Varela, Brown, Antonio, Biesel, Steel and Brown (1995) Nature (London) 374, 62-64]. The myosin VIIA gene is expressed in hair cells in the cochlea, where it is thought to function in the development of the critical neuroepithelium where auditory transduction takes place. In order to understand better the function of myosin VIIA, we have determined the complete sequence of the mouse myosin VIIA cDNA and employed the wild-type sequence for mutational analysis of a number of shaker-1 alleles. Analysis of the mouse myosin VIIA tail sequence demonstrates a large internal repeat with regions of similarity to myosins IV, X and XII as well as members of the band 4.1 family. In addition, the myosin VIIA repeats are similar along their entire length to a tail domain from a plant kinesin. The mouse myosin VIIA tail also contains a putative Src homology 3 (SH3) domain. Along with three previously reported shaker-1 mutations, mutations for seven shaker-1 alleles in total have now been identified. The mutational changes have been analysed in terms of their predicted effect on both myosin motor head and tail domain function and the predictions related to the known phenotypes of the shaker-1 alleles. Five of the mutations lie in the motor head, and analysis of their likely effect on myosin head structure correlates well with the known severity of the shaker-1 alleles. Of the two mutations in the tail, one is a missense mutation within the kinesin and myosin IV, X and XII homology domains that substitutes a conserved amino acid and leads to a severe deafness phenotype. This and other data suggest that myosin VIIA may have properties of a myosin-motor-kinesin-tail hybrid and be involved in membrane turnover within the actin-rich environment of the apical hair cell surface.


Assuntos
Análise Mutacional de DNA , Surdez/genética , Miosinas/genética , Sequência de Aminoácidos , Animais , Clonagem Molecular , DNA Complementar/genética , Dineínas , Genes/genética , Camundongos , Camundongos Mutantes Neurológicos , Modelos Moleculares , Dados de Sequência Molecular , Miosina VIIa , Miosinas/química , RNA Mensageiro/genética , Sequências Repetitivas de Ácido Nucleico/genética , Alinhamento de Sequência , Homologia de Sequência do Ácido Nucleico , Transcrição Gênica/genética , Domínios de Homologia de src
13.
Structure ; 4(8): 969-87, 1996 Aug 15.
Artigo em Inglês | MEDLINE | ID: mdl-8805581

RESUMO

BACKGROUND: Myosins are motors that use energy supplied by ATP to travel along actin filaments. The structure of myosin is known, but the actin-binding site is not well defined, and the mechanisms by which actin activates ATP hydrolysis by myosin, and myosin moves relative to the actin filament, developing force, are not fully understood. Previous phylogenetic analyses of the motor domain of myosins have identified up to twelve classes. We set out to analyse the positions of conserved residues within this domain in detail, and relate the conserved residues to the myosin structure. RESULTS: Our analysis indicates that there are at least thirteen myosin classes. Conserved residues in the motor domain have been positioned within the framework provided by the recent crystal structures, thus helping to define those residues involved in actin and ATP binding, in hydrolysis and in conformational change. This has revealed remarkably poor overall conservation at the site thought to be involved in actin binding, but several highly conserved residues have been identified that may be functionally important. CONCLUSIONS: Information from such a sequence analysis is a useful tool in the further interpretation of X-ray structures. It allows the position of crucial residues from other members of a superfamily to be determined within the framework provided by the known structures and the functional significance of conserved or mutated residues to be assessed.


Assuntos
Actinas/metabolismo , Trifosfato de Adenosina/metabolismo , Miosinas/química , Estrutura Terciária de Proteína , Sequência de Aminoácidos , Grupos de População Animal/genética , Grupos de População Animal/metabolismo , Animais , Formação de Anticorpos , Galinhas/metabolismo , Sequência Consenso , Cristalografia por Raios X , Epitopos/química , Epitopos/imunologia , Evolução Molecular , Hidrólise , Modelos Moleculares , Dados de Sequência Molecular , Miosinas/genética , Miosinas/imunologia , Miosinas/metabolismo , Filogenia , Proteínas de Plantas/química , Proteínas de Plantas/genética , Proteínas de Plantas/fisiologia , Plantas/genética , Plantas/metabolismo , Ligação Proteica , Alinhamento de Sequência , Homologia de Sequência de Aminoácidos , Especificidade da Espécie , Relação Estrutura-Atividade
16.
Nurs Res ; 24(2): 138-44, 1975.
Artigo em Inglês | MEDLINE | ID: mdl-1038618

RESUMO

Patient care scores of staff nurses in seven Veterans Administration hospitals who used a performance counseling protocol that required written goal setting, coupled with head nurse modeling and support to achieve goals (experimental), were compared with scores of nurses who continued with usual practice (control). Staff nurses chose their own goals. One goal was to improve patient care and the other was to improve staff nurse professional competence. After six months, experimental group scores were higher on five patient care scales, one significantly. After 12 months, scores shifted in favor of the control group, one significantly. Experimental group scores were higher on patient interview questions after six months and made additional gains after 12 months. Experimental nurses generally were more satisfied with their nursing careers and described working relationships more positively. Some progress the experimental nurses made after six months was lost after 12 months. Nurses who received high patient care scores from outside observers described the hospital working environment in more positive terms. Relationships of three instruments that measure quality of patient care are presented.


Assuntos
Objetivos , Motivação , Cuidados de Enfermagem/normas , Encaminhamento e Consulta , Logro , Hospitais de Veteranos , Humanos , Serviço Hospitalar de Enfermagem , Recursos Humanos de Enfermagem Hospitalar , Supervisão de Enfermagem , Satisfação Pessoal , Testes Psicológicos , Qualidade da Assistência à Saúde , Desempenho de Papéis , Meio Social , Fatores de Tempo , Estados Unidos
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