Biomedical subjects

H Li

Publications and source records attributed to H Li.

At least 523 records · Page 29Linked to original sources

PubMed2000

The t(5;17) acute promyelocytic leukemia fusion protein NPM-RAR interacts with co-repressor and co-activator proteins and exhibits both positive and negative transcriptional properties.

The t(5;17) variant of acute promyelocytic leukemia (APL) fuses the genes for nucleophosmin (NPM) and the retinoic acid receptor alpha (RARalpha). Two NPM-RAR molecules are expressed as a result of alternative RNA splicing. Both contain RARalpha sequences that encode the DNA binding, heterodimerization, and ligand activation domains of RARalpha. This study was designed to test the ability of these fusion proteins to act as transcriptional activators of retinoic acid responsive promoters. The NPM-RAR fusion proteins bind to retinoic acid response element sequences as either homodimers or as heterodimers with RXR. Transcription of retinoic acid-inducible promoters is activated by the fusion proteins in the presence of retinoic acid. The level of transactivation induced by the NPM-RAR fusions differs from the level of transactivation induced by wild-type RARalpha in both a promoter and cell specific fashion, and more closely parallels the pattern of activation of the PML-RAR fusion than wild-type RARalpha. In addition, NPM-RAR decreases basal transcription from some promoters and acts in a dominant-negative fashion when co-transfected with wild-type RARalpha. Both NPM-RAR and PML-RAR interact with the co-repressor protein SMRTe in a manner that is less sensitive than RARalpha to dissociation by retinoic acid. Retinoic acid induces binding of the co-activator protein RAC3. These data indicate that the NPM-RAR fusion proteins can modulate expression of retinoid-responsive genes in a positive or negative manner, depending on context of the promoter, and lend support to the hypothesis that aberrant transcriptional activation underlies the APL phenotype. (Blood. 2000;95:2683-2690)

Chromosomes, Human, Pair 17↗

PubMed2000

Genetic modification of survival in tissue-specific knockout mice with mitochondrial cardiomyopathy.

We recently described a mouse model that reproduces important pathophysiological features of mitochondrial DNA (mtDNA) mutation diseases. The gene for mouse mitochondrial transcription factor A, Tfam (also called mtTFA), a nucleus-encoded key regulator of mtDNA expression, was targeted with loxP sites (Tfam(loxP)) and disrupted in vivo by transgenic expression of cre-recombinase from the muscle creatinine kinase (Ckmm) promoter. This promoter is active from embryonic day 13, and the knockouts had normal respiratory chain function in the heart at birth and developed mitochondrial cardiomyopathy postnatally. In this paper, we describe a heart-knockout strain obtained by mating Tfam(loxP) mice to animals expressing cre-recombinase from the alpha-myosin heavy chain (Myhca) promoter. This promoter is active from embryonic day 8, and the knockouts had onset of mitochondrial cardiomyopathy during embryogenesis. The age of onset of cardiac respiratory chain dysfunction can thus be controlled by temporal regulation of cre-recombinase expression. Further characterization demonstrated that approximately 75% of the knockouts died in the neonatal period, whereas, surprisingly, approximately 25% survived for several months before dying from dilated cardiomyopathy with atrioventricular heart conduction blocks. Modifying gene(s) affect the life span of the knockouts, because approximately 95% of the knockout offspring from an intercross of the longer-living knockouts survived the neonatal period. Thus, the tissue-specific knockouts we describe here not only reproduce important pathophysiological features of mitochondrial cardiomyopathy but also provide a powerful system by which to identify modifying genes of potential therapeutic value.

Animals↗

PubMed2000

Rapid internal dynamics of BPTI is insensitive to pressure. (15)N spin relaxation at 2 kbar.

Pressure effects on the backbone dynamics of a native basic pancreatic trypsin inhibitor (BPTI) have been measured by (15)N spin relaxation and chemical shifts at 30 and 2000 bar. The experiments utilized the on-line variable pressure cell nuclear magnetic resonance system on (15)N-uniformly labeled BPTI at a proton frequency of 750.13 MHz at 36 degrees C. Longitudinal (R(1)) and transverse (R(2)) (15)N relaxation times and ((1)H)-(15)N nuclear Overhauser effects were measured for 41 protonated backbone nitrogens at both pressures. The model free analysis of the internal dynamics gave order parameters for individual H-N vectors at both pressures. The results indicate that rapid internal dynamics in the ps-ns range for the polypeptide backbone is not significantly affected by pressure in the range between 30 bar and 2 kbar. The result is consistent with the linear pressure dependence of (1)H and (15)N chemical shifts of BPTI, which suggests that local compressibilities and amplitudes of associated conformational fluctuation are nearly invariant in the same pressure range. Overall, we conclude that at 2 kbar BPTI remains within the same native ensemble as at 1 bar, with a small shift of population from that at 1 bar.

Aprotinin↗

PubMed2000

Spatial and temporal patterns of transneuronal labeling in CNS neurons after injection of pseudorabies virus into the sciatic nerve of adult rats.

The distribution of labeled neurons in the brain and spinal cord was studied after injecting the Bartha strain of pseudorabies virus (PRV) into the sciatic nerve to provide a baseline for studying neural circuitry after spinal cord injury (SCI) and regeneration. Following a single injection of viral particles into the left sciatic nerve, PRV labeling was found in the spinal cord at 2 days post-injection (p.i.). Increasing complexity in viral labeling from the spinal cord to supraspinal regions became apparent with increasing survival time. In brain regions, several neuronal groups that regulate sympathetic outflow, such as the rostroventrolateral medulla, the lateral paragigantocellular nuclei, and the A5 cells, were densely labeled. However, relatively sparse labeling was noticed in the lateral vestibular nuclei, the red nucleus and the motor cortex whose spinal projections regulate somatic motor function, although those areas were abundantly labeled with Fast blue (FB) in a double-labeling experiment in which FB was co-injected into the lumbar cord. The pattern of viral labeling became more complex beyond 5 days p.i. when increased numbers of cell groups were labeled with PRV but not FB. In addition, some infected neurons started to lyse, as evidenced by a decrease in viral labeling at 7 days p.i. Thus, the 5th day post-viral injection would appear to be an appropriate survival time to obtain maximal labeling with acceptable specificity. We suggest that transneuronal labeling using PRV should be appropriate for studying multi-neural circuitry after SCI and regeneration.

Amidines↗

PubMed2000

Differential mechanisms of nuclear receptor regulation by receptor-associated coactivator 3.

Steroid and nuclear receptor coactivators (NCoAs) have been implicated in the regulation of nuclear receptor function by enhancing ligand-dependent transcriptional activation of target gene expression. We have previously isolated receptor-associated coactivator 3 (RAC3), which belongs to the steroid receptor coactivator family. In this study, we investigated the differential mechanisms by which RAC3 interacts with and modulates the transcriptional activity of different nuclear receptors. We found that the vitamin D receptor (VDR) and estrogen receptor beta interact with different alpha-helical LXXLL motifs of RAC3. Peptides corresponding to these motifs have diverse affinities for the VDR and estrogen receptor beta, and mutation of specific motifs differentially impairs the ability of RAC3 to interact with these receptors in vitro. Consequently, these mutations inhibit the enhancement of transcriptional activation by these receptors in vivo. Furthermore, we found that the activation function-2 (AF-2) domain of the retinoid X receptor interferes with RAC3 binding to a DNA-bound VDR/retinoid X receptor (RXR) heterodimer, whereas the VDR AF-2 domain is required for this interaction. These results suggest a receptor-specific binding preference for the different LXXLL motifs of RAC3, which may provide flexibility for RAC3 to differentially regulate the function of different nuclear receptors.

Amino Acids↗

PubMed2000

Ectopic G-protein expression in dopamine and serotonin neurons blocks cocaine sensitization in Drosophila melanogaster.

Sensitization to repeated doses of psychostimulants is thought to be an important component underlying the addictive process in humans [1] [2] [3] [4]. In all vertebrate animal models, including humans [5], and even in fruit flies, sensitization is observed after repeated exposure to volatilized crack cocaine [6]. In vertebrates, sensitization is thought to be initiated by processes occurring in brain regions that contain dopamine cell bodies [2] [7]. Here, we show that modulated cell signaling in the Drosophila dopamine and serotonin neurons plays an essential role in cocaine sensitization. Targeted expression of either a stimulatory (Galpha(s)) or inhibitory (Galpha(i)) Galpha subunit, or tetanus toxin light chain (TNT) in dopamine and serotonin neurons of living flies blocked behavioral sensitization to repeated cocaine exposures. These flies showed alterations in their initial cocaine responsiveness that correlated with compensatory adaptations of postsynaptic receptor sensitivity. Finally, repeated drug stimulation of a nerve cord preparation that is postsynaptic to the brain amine cells failed to induce sensitization, further showing the importance of presynaptic modulation in sensitization.

Animals↗

PubMed2000

Analysis of the mRNA transcripts of the survival motor neuron (SMN) gene in the tissue of an SMA fetus and the peripheral blood mononuclear cells of normals, carriers and SMA patients.

Spinal muscular atrophy (SMA) is a disorder characterized by degeneration of the anterior horn cells of the spinal cord. The gene most highly associated with SMA is the survival motor neuron (SMN) gene. In this study, we present an analysis of messenger RNA (mRNA) expression of the SMN gene in peripheral blood mononuclear cells in normal subjects, SMA carriers and patients from 20 SMA families. We found at least 6-8 different transcripts of SMN gene formed by alternative splicing involving exons 3, 5 and 7. We compared transcripts from the different types of SMA and found no definite differences in transcript patterns and amounts. Normal subjects with the telomeric SMN (SMN(T)) gene only had variable splicing resulting in several transcripts, the most dominant being a transcript containing all coding regions. However, SMA patients with the centromeric SMN (SMN(C)) gene only had a higher degree of splice variation and tended to show little or no exon 7. These results demonstrate that SMN(T) and SMN(C) genes participate in alternative splicing phenomena. The different splicing patterns support the view that the SMN(T) gene is responsible for SMA disease. We also analyzed the transcripts from several tissues of an SMA fetus who had a homozygous SMN(T) gene deletion. Different splicing patterns were also found in these tissues, and were similar to the splicing pattern of leukocytes. We compared the major transcripts from exons 4 to 8 of both the SMN(T) and SMN(C) genes and found that the relative proportion varied among normal subjects, SMA carriers and patients. This approach could be used as a novel diagnostic method. We suggest that analyzing the mRNA expression of the SMN gene in peripheral blood mononuclear cells offers an apparently reliable technique for separating SMA patients, carriers, and normal individuals.

Adult↗

PubMed2000

Direct stereoselective synthesis of beta-thiomannosides.

A highly diastereoselective synthesis of beta-thiomannopyranosides is described in which S-phenyl 2,3-di-O-benzyl-4, 6-O-benzylidene-1-deoxy-1-thia-alpha-D-mannopyranoside S-oxide is treated with triflic anhydride and 2, 6-di-tert-butyl-4-methylpyridine in CH(2)Cl(2) at -78 degrees C leading to the formation of an intermediate alpha-mannosyl triflate. Addition of primary, secondary, or tertiary thiols then leads to the beta-thiomannosides, by an S(N)2-like displacement, in good yield and with excellent stereoselectivity. Deprotection is achieved either by Birch reduction or by Zemplen deacetylation, of the acetyl protected aglycons, followed by hydrogenolysis over Pearlman's catalyst. The assignment of configuration of the beta-thiomannopyranosides is discussed in terms of the chemical shift of the mannose H5 resonance and the (1)J(CH) of the mannose anomeric carbon.

Carbohydrate Conformation↗

PubMed2000

Neuroprotection achieved with a novel proteasome inhibitor which blocks NF-kappaB activation.

Activated NF-kappaB contributes to cerebral infarction by triggering a neuro-inflammatory response. Rats subjected to 90min middle cerebral artery occlusion developed a cortical infarct of 20+/-4% of hemispheric volume (n = 8). Treatment with the proteasome inhibitor CVT-634 resulted in a significantly smaller infarct of 13+/-2% (n = 7, p<0.01) and 12+/-2% (n = 8, p<0.001) of hemispheric volume at 1 day and 7 days, respectively. Since regional cerebral blood flows for the core and penumbral regions were not affected, we concluded that all animals received the same ischemic insult The reduction in infarction persisted for 7 days. This is the first indication that a proteasome inhibitor can reduce infarct volume in a focal model of cerebral ischemia.

Animals↗

PubMed2000

[Combined effects of lead and ethanol on rat sperms].

In order to study the combined effects of lead and ethanol on rat sperm, 54 male rats were divided into 9 groups randomly. One group was given distilled water as control, and the others (A-H) groups were given lead and ethanol at the concentrations of lead 11 mg/kgBW and lead 22 mg/kgBW, ethanol 0.9 g/kgBW, ethanol 1.8 g/kgBW, lead 11 mg/kgBW + ethanol 0.9 g/kgBW, lead 11 mg/kgBW + ethanol 1.8 g/kgBW, lead 22 mg/kgBW + ethanol 0.9 g/kgBW, lead 22 mg/kgBW + ethanol 1.8 g/kgBW in stomachs respectively for four weeks. The rats were sacrificed by the end of the fourth week. Epididymis were isolated and examined for sperm motility, counts and morphology. The results showed that the spermatozoa motility as well as spermatozoa count was lower; the spermatozoa morphological changed and blood lead level and ratio of epididymis to weight were higher in all combined experimental groups than those in groups with lead or ethanol alone. ANOVA analysis indicated that there were interaction between lead and ethanol on above indices (P < 0.05 P < 0.01). The multiple linear regression showed that there was linear correlation between blood lead and spermatozoa motility, spermatozoa morphological change. It is concluded that there were notable combined effects of lead and ethanol on semen quality in male rats.

Animals↗

PubMed2000

[Effect of fish oil supplementation on fatty acid composition and neurotransmitters of growing rats].

In order to observe the change of brain fatty acid composition and neurotransmitter by DHA supplementation during the development stage of young rats, pregnant rats were randomly divided into four groups: normal control group (O), low (L), medium (M) and high (H) dose-DHA supplemented groups. The fatty acids composition, the levels of 5-hydroxy-tryptamine (5-HT), dopamine (DA), norepinephrine (NE) and somatostatin (SS) in ceretral cortex and hippocampus of offsprings were measured. The body weight of pregnant rats and offsprings were also observed. The results showed that DHA content of brain homogenate and the levels of 5-HT, DA and SS in hippocampus of experimental young rats were significantly higher than those of the control group. And the body weight of young rats in the three DHA-supplemented groups were retarded in different degree. It was concluded that DHA supplementation changed the fatty acid composition and increased the levels of 5-HT, DA and SS in hippocampus. Proper ratio of n-3 and n-6 fatty acids in dietary supplementation should be considered.

Animals↗

PubMed2000

Cloning and characterization of IL-17B and IL-17C, two new members of the IL-17 cytokine family.

IL-17 is a T cell-derived cytokine that may play an important role in the initiation or maintenance of the proinflammatory response. Whereas expression of IL-17 is restricted to activated T cells, the IL-17 receptor is found to be widely expressed, a finding consistent with the pleiotropic activities of IL-17. We have cloned and expressed two novel human cytokines, IL-17B and IL-17C, that are related to IL-17 ( approximately 27% amino acid identity). IL-17B mRNA is expressed in adult pancreas, small intestine, and stomach, whereas IL-17C mRNA is not detected by RNA blot hybridization of several adult tissues. No expression of IL-17B or IL-17C mRNA is found in activated T cells. In a survey of cytokine induction, IL-17B and IL-17C stimulate the release of tumor necrosis factor alpha and IL-1beta from the monocytic cell line, THP-1, whereas IL-17 has only a weak effect in this system. No induction of IL-1alpha, IL-6, IFN-gamma, or granulocyte colony-stimulating factor is found in THP-1 cells. Fluorescence-activated cell sorter analysis shows that IL-17B and IL-17C bind to THP-1 cells. Conversely, IL-17B and IL-17C are not active in an IL-17 assay or the stimulation of IL-6 release from human fibroblasts and do not bind to the human IL-17 receptor extracellular domain. These data show that there is a family of IL-17-related cytokines differing in patterns of expression and proinflammatory responses that may be transduced through a cognate set of cell surface receptors.

Amino Acid Sequence↗

PubMed2000

Potential risk of vasovagal syncope for motor vehicle driving.

Vasovagal syncope is the most common cause of syncope, but its risk for driving remains uncertain. We analyzed the clinical characteristics of patients who had syncope during driving and subsequently underwent the head-up tilt test (HUTT). Of the 245 consecutive patients undergoing HUTT, 23 (9%) had > or =1 episode of syncope during driving. HUTT was positive in 19 (group A) and negative in 4 (group B) patients. No patient had structural heart disease. In group A, the driving incident occurred on the first syncope in 3 patients, and the other 16 patients had 1 to 4 episodes of prior syncope not associated with driving. In group B, the driving incident occurred on the first syncope in 1 patient, and the other 3 patients had prior syncope (3 episodes in each) not associated with driving. Seven group A and 1 group B patients had 2 syncope-related driving incidents, and the remaining patients had only 1 syncope-related driving incident. The syncope-related driving incidents caused personal injury in 7 group A and 2 group B patients. One incident in 1 group A patient caused the death of another driver. After HUTT, all but 1 patient in group A received medical treatment and only 1 patient in group B received empirical beta-blocker therapy. During the follow-up of 51+/-26 months, 1 patient died and another was lost to follow-up. Of the remaining patients, 4 patients had recurrence of syncope and 2 patients had presyncope in group A. One of these patients had another syncope-related driving incident. No group B patient had syncope recurrence. A second etiology of syncope was never found in any patient. We conclude that vasovagal syncope during driving is not uncommon in patients referred for syncope evaluation. Early medical attention to patients with vasovagal syncope may help reduce syncope-related driving incidents.

Adolescent↗

PubMed2000

Effects of long-term nitroglycerin treatment on endothelial nitric oxide synthase (NOS III) gene expression, NOS III-mediated superoxide production, and vascular NO bioavailability.

Long-term nitroglycerin (NTG) treatment has been shown to be associated with cross-tolerance to endothelium-dependent vasodilators. It may involve increased production of reactive oxygen species (such as superoxide, O(2)(.-)) that rapidly inactivate the nitric oxide (NO) released from the endothelial cells. It remains to be elucidated, however, whether long-term treatment with NTG alters the activity and expression of the endothelial NO synthase (NOS III) and whether this enzyme can contribute to O(2)(.-) formation. We studied the influence of long-term NTG treatment on the expression of NOS III as assessed by RNase protection assay and Western blot. Tolerance was measured ex vivo in organ chamber experiments with rat aortic rings. O(2)(.-) and NO formation were quantified using lucigenin- and Cypridina luciferin analog-enhanced chemiluminescence as well as electron spin resonance (ESR) spectroscopy. Treatment of Wistar rats with NTG (Alzet osmotic minipumps, NTG concentration 10 microg x kg(-1) x min(-1)) for 3 days caused marked tolerance, cross-tolerance to the endothelium-dependent vasodilator acetylcholine, and a significant increase in O(2)(.-)-induced chemiluminescence. Tolerance was associated with a significant increase in NOS III mRNA to 236+/-28% and NOS III protein to 239+/-17%. In control vessels, the NOS inhibitor N(G)-nitro-L-arginine (L-NNA) increased the O(2)(.-)-mediated chemiluminescence, indicating that basal production of endothelium-derived NO depresses the baseline chemiluminescence signal. In the setting of tolerance, however, L-NNA decreased steady-state O(2)(.-) levels, indicating the involvement of NOS III in O(2)(.-) formation. Likewise, A23187-induced, NOS III-mediated O(2)(.-) production was more pronounced in tolerant than in control vessels. Vascular NO bioavailability as assessed with ESR spectroscopy using iron-thiocarbamate as a trap for NO was significantly reduced in tolerant vessels. Pretreatment of tolerant tissue in vitro with the protein kinase C (PKC) inhibitors reduced basal and stimulated NOS III-mediated O(2)(.-) production and partially reversed vascular tolerance. These findings suggest that NTG treatment increases the expression of a dysfunctional NOS III gene, leading to increased formation of O(2)(.-) and decreased vascular NO bioavailability. Normalization of NOS III-mediated O(2)(. -) production and improvement of tolerance with PKC inhibition suggests an important role for PKC isoforms in mediating vascular dysfunction caused by long-term NTG treatment.

Acetylcholine↗

PubMed2000

Surface expression of Rh-associated glycoprotein (RhAG) in nonerythroid COS-1 cells.

In the Rh blood system, RhAG (Rh-associated glycoprotein, or Rh50) is thought to be involved in Rh30 (D, CE) expression by forming a protein complex on the red cell surface. To obtain further insight into the Rh complex, we chose nonerythroid COS-1 cells instead of proerythroblast-like K562 cells, which produce endogenous Rh proteins as cell host, for the expression of both RhAG and RhD. The RhAG cDNA was subcloned into a retroviral vector, and a stable COS-1 cell line was then established via retroviral transduction. Surface expression of RhAG on the COS-1 cells was monitored by flow cytometry using mouse monoclonal anti-RhAG(2D10). Under these conditions, we detected significant expression of RhAG on the cell surface, compared to stable COS-1 cells transduced with the vector alone. To confirm the results, we isolated RhAG by immunoprecipitation from the lysate of the COS-1 cells, which were metabolically labeled with [(35)S]-methionine. A strong band of the 32 kd on SDS-PAGE was obtained, corresponding to the results obtained from other cultured cells (K562 cell and others), which always produce partially glycosylated RhAG with a molecular weight of 32 kd. Thus, RhAG was expressed without Rh30 and other Rh-related glycoproteins (LW, glycophorin B) in nonerythroid cells. Using the same strategy, however, we could not express RhD epitopes on COS-1 cells even in the presence of RhAG cDNA, suggesting that other factors might be required for the surface expression of RhD antigen. (Blood. 2000;95:336-341)

Animals↗

PubMed2000

Nitric oxide in the pathogenesis of vascular disease.

Nitric oxide (NO) is synthesized by at least three distinct isoforms of NO synthase (NOS). Their substrate and cofactor requirements are very similar. All three isoforms have some implications, physiological or pathophysiological, in the cardiovascular system. The endothelial NOS III is physiologically important for vascular homeostasis, keeping the vasculature dilated, protecting the intima from platelet aggregates and leukocyte adhesion, and preventing smooth muscle proliferation. Central and peripheral neuronal NOS I may also contribute to blood pressure regulation. Vascular disease associated with hypercholesterolaemia, diabetes, and hypertension is characterized by endothelial dysfunction and reduced endothelium-mediated vasodilation. Oxidative stress and the inactivation of NO by superoxide anions play an important role in these disease states. Supplementation of the NOS substrate L-arginine can improve endothelial dysfunction in animals and man. Also, the addition of the NOS cofactor (6R)-5,6,7, 8-tetrahydrobiopterin improves endothelium-mediated vasodilation in certain disease states. In cerebrovascular stroke, neuronal NOS I and cytokine-inducible NOS II play a key role in neurodegeneration, whereas endothelial NOS III is important for maintaining cerebral blood flow and preventing neuronal injury. In sepsis, NOS II is induced in the vascular wall by bacterial endotoxin and/or cytokines. NOS II produces large amounts of NO, which is an important mediator of endotoxin-induced arteriolar vasodilatation, hypotension, and shock.

Cardiovascular Diseases↗

PubMed2000

Validation of biomarkers in humans exposed to benzene: urine metabolites.

BACKGROUND: The present study was conducted among Chinese workers employed in glue- and shoe-making factories who had an average daily personal benzene exposure of 31+/-26 ppm (mean+/-SD). The metabolites monitored were S-phenylmercapturic acid (S-PMA), trans, trans-muconic acid (t,t-MA), hydroquinone (HQ), catechol (CAT), 1,2, 4-trihydroxybenzene (benzene triol, BT), and phenol. METHODS: S-PMA, t,t-MA, HQ, CAT, and BT were quantified by HPLC-tandem mass spectrometry. Phenol was measured by GC-MS. RESULTS: Levels of benzene metabolites (except BT) measured in urine samples collected from exposed workers at the end of workshift were significantly higher than those measured in unexposed subjects (P < 0.0001). The large increases in urinary metabolites from before to after work strongly correlated with benzene exposure. Concentrations of these metabolites in urine samples collected from exposed workers before work were also significantly higher than those from unexposed subjects. The half-lives of S-PMA, t,t-MA, HQ, CAT, and phenol were estimated from a time course study to be 12.8, 13.7, 12.7, 15.0, and 16.3 h, respectively. CONCLUSIONS: All metabolites, except BT, are good markers for benzene exposure at the observed levels; however, due to their high background, HQ, CAT, and phenol may not distinguish unexposed subjects from workers exposed to benzene at low ambient levels. S-PMA and t,t-MA are the most sensitive markers for low level benzene exposure.

Acetylcysteine↗

PubMed2000

Families and hospitalized elders: A typology of family care actions.

The extensive care provided by families to their elderly relatives in the home is well documented. Although family caregiving is likely to be continued during hospitalization of elderly relatives, limited research has been conducted to address the nature of family care for hospitalized elders. The main purpose of this qualitative study was to refine the content domain of family care for hospitalized elders. Altogether 25 interviews were done. Of the 16 participants, 6 were family members, 6 were patients, and 4 were nurses; 7 participants were interviewed once and 9 participants were interviewed twice. Qualitative analysis based on Lofland and Lofland's (1984, 1995) approach resulted in the identification of three major content domains: family members providing care to the patient, working together with the health care team, and taking care of themselves. This typology suggests a shift of research in this area from its current focus on family needs to a view of family caregivers as partners with the health care team.

Aged↗