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PubMed2006

Fanconi's anaemia and related bone marrow failure syndromes.

The inherited bone marrow (BM) failure syndromes are a heterogeneous group of disorders characterized by BM failure, usually in association with one or more somatic abnormalities. The BM failure may present at birth or at a variable time thereafter including in adulthood in some cases. Over the last decade, there have been significant advances in the genetics of these syndromes particularly Fanconi's anaemia (FA) and dyskeratosis congenita (DC). These advances are beginning to provide a better understanding of normal haemopoiesis and of the pathophysiology of some cases of idiopathic aplastic anaemia (AA). They have also provided important insights into some aspects of DNA repair (FA/BRCA pathway) and telomere maintenance (DC-related genes), two pathways critical in the maintenance of genomic stability. These advances are already facilitating better diagnosis of patients with these disorders. It is hoped that they will also form the basis for developing new treatments.

Anemia, Diamond-Blackfan↗
PubMed1997

Evidence for cytochrome P450 2A6 and 3A4 as major catalysts for N'-nitrosonornicotine alpha-hydroxylation by human liver microsomes.

The tobacco specific carcinogen N'-nitrosonornicotine (NNN), is believed to be a causative agent for esophageal cancer in smokers. NNN requires metabolic activation to exert its carcinogenic potential. Metabolism occurs through cytochrome P450 (P450) catalyzed 2'- and 5'-hydroxylation, which generates unstable metabolites that decompose to 4-hydroxy-1-(3-pyridyl)-1-butanone ('keto alcohol') and 4-hydroxy-4-(3-pyridyl)butanal, respectively. The latter cyclyzes to 5-(3-pyridyl)-2-hydroxytetrahydrofuran ('lactol'). 2'-Hydroxylation of NNN is believed to be the pathway critical for esophogeal NNN carcinogenesis in the rat. The ability of human liver microsomes and expressed human P450s to metabolize [5-(3)H]NNN to keto alcohol and lactol was determined by reverse phase HPLC with radioflow detection. At low NNN concentrations, 11 human liver microsomes metabolized NNN primarily by 5'-hydroxylation to lactol. This reaction was strongly correlated (r = 0.92) with coumarin 7-hydroxylation, suggesting that NNN 5'-hydroxylation is catalyzed mainly by P450 2A6. 2'-Hydroxylation of NNN by human liver microsomes correlated with 6beta-hydroxylation of testosterone, a P450 3A4-specific activity (r = 0.94). The relative rates of 2'- and 5'-hydroxylation by human P450s 2A6, 2E1, 2D6 and 3A4 expressed in Sf9 cells by the baculovirus-insect cell expression system, and human P450 3A4 produced by stable expression in Chinese hamster ovary cells, were determined. Human P450 2A6 metabolized 1 microM NNN exclusively by 5'-hydroxylation. The rate of lactol formation was 317 pmol/min per nmol P450. Human P450s 2E1 and 2D6 also metabolized NNN only to lactol, but at much lower rates, 0.4 and 0.8 pmol/min per nmol of P450 respectively. In contrast, the metabolism of NNN by expressed human P450 3A4 was specific for keto alcohol formation. The Km for 5'-hydroxylation by baculovirus-expressed P450 2A6 was 2.1 microM, and k(cat) was 953 pmol/min per nmol of P450. The Km for lactol formation by human liver microsomes containing high levels of P450 2A6, was 5 microM . Human liver microsomes exhibited a Km of 312 microM for keto alcohol formation. Coumarin, 8-methoxypsoralen (P450 2A6 inhibitors), and anti-2A6 monoclonal antibody were strong inhibitors of NNN-derived lactol formation in human liver microsomes. Troleandomycin, an inhibitor of P450 3A4, effectively inhibited the metabolism of NNN to keto alcohol by human liver microsomes. These results are consistent with P450 2A6 mediated 5'-hydroxylation and P450 3A4 mediated 2'-hydroxylation of NNN in human liver microsomes.

Animals↗
PubMed1998

2,3-epoxy-4-hydroxynonanal, a potential lipid peroxidation product for etheno adduct formation, is not a substrate of human epoxide hydrolase.

Our previous studies have shown that 2,3-epoxy-4-hydroxynonanal, a reactive epoxy aldehyde capable of forming etheno adducts with DNA bases, is mutagenic and tumorigenic (Carcinogenesis, 14, 2073). The epoxy aldehyde can be generated from trans-4-hydroxy-2-nonenal, a lipid peroxidation product of omega-6 polyunsaturated fatty acids, by autoxidation or by incubation with fatty acid hydroperoxides or hydrogen peroxides (Chem. Res. Toxicol., 9, 306). These are plausible in vivo pathways for the formation of 2,3-epoxy-4-hydroxynonanal. The possibility that 2,3-epoxy-4-hydroxynonanal is a tumorigen of endogenous origin is suggested by recent observations that etheno bases are detected as background DNA lesions in untreated rodents and humans. A metabolic pathway critical for detoxification of 2,3-epoxy-4-hydroxynonanal involves the ring-opening by epoxide hydrolase, which abolishes its ability to form cyclic etheno DNA adducts. In this study, we examined whether 2,3-epoxy-4-hydroxynonanal is a substrate of cDNA expressed human epoxide hydrolase. Human epoxide hydrolase was expressed in TK- 143 cells (thymidine kinase-deficient human embryoblast) infected with recombinant vaccinia virus encoding human epoxide hydrolase cDNA. Controls consisted of the cells infected with vaccinia virus in the absence of human epoxide hydrolase cDNA. No hydrolysis occurred when [2,3-(3)H]2,3-epoxy-4-hydroxynonanal was incubated at 37 degrees C for 30 min at pH 7.4 with cells expressing human epoxide hydrolase, as indicated by the presence of a pair of radioactive peaks in reversed-phase HPLC chromatography, which comigrated with the UV standards of the two diastereomers of the epoxy aldehyde. The identity of these compounds as the intact epoxy aldehyde was further supported by derivatization to the 2,4-dinitrophenylhydrazones followed by reversed phase HPLC analysis. Similar results were observed with the control cells or with the heat deactivated human epoxide hydrolase. The epoxide hydrolase activity in the expressed cells was demonstrated by their ability to convert benzo[a]pyrene-4,5-dihydroepoxide to benzo[a]pyrene-trans-4,5-dihydrodiol under the same conditions. These results clearly indicate that 2,3-epoxy-4-hydroxynonanal is not a substrate of human epoxide hydrolase, and, thus strengthen its possible endogenous role in the formation of promutagenic exocyclic etheno adducts in vivo.

Aldehydes↗
PubMed1998

Effects of Cr(VI) on the expression of the oxidative stress genes in human lung cells.

Intracellular metabolism of chromium(VI) [Cr(VI)] may lead to oxidative stress and this may account for the ability of Cr(VI) to act as a complete carcinogen. Therefore, we examined the effects of Cr(VI) treatment on the expression of oxidative stress genes in normal human lung LL 24 cells and human lung adenocarcinoma A549 cells. RT-PCR and northern blot analyses were used to determine the steady-state mRNA levels of catalase, glutathione S-transferase, glutathione reductase, Cu/Zn- and Mn-superoxide dismutases, glutathione peroxidase, NAD(P)H:quinone oxidoreductase, heme oxygenase and interleukin 8 in control cells and cells treated with 5-200 microM of Cr(VI). We found that only expression of the heme oxygenase gene is strongly elevated under the treatment with Cr(VI), and only in normal human lung LL 24 cells. Our data showed that even in the absence of Cr(VI) treatment, the level of heme oxygenase gene expression is much higher in A549 cells than in LL 24 cells. As glutathione is believed to play a protective role in cells against different forms of oxidative stress, we studied the correlation between intracellular glutathione levels and the inducibility of the heme oxygenase gene after treatment of cells with Cr(VI). Our results demonstrate that glutathione levels are increased by 35 % of control values in LL 24 cells treated with Cr(VI). The data obtained indicate that heme oxygenase, known to be a stress-inducible gene, may be involved in cellular pathways critical to the carcinogenic activity of Cr(VI) in normal human lung cells. Intracellular glutathione levels and reactive oxygen species do not appear to be primarily responsible for the stress response, induced by Cr(VI) in the studied human cells.

Acetylcysteine↗
PubMed1997

The cardiac transcription factors Nkx2-5 and GATA-4 are mutual cofactors.

The tissue-restricted GATA-4 transcription factor and Nkx2-5 homeodomain protein are two early markers of precardiac cells. Both are essential for heart formation, but neither can initiate cardiogenesis. Overexpression of GATA-4 or Nkx2-5 enhances cardiac development in committed precursors, suggesting each interacts with a cardiac cofactor. We tested whether GATA-4 and Nkx2-5 are cofactors for each other by using transcription and binding assays with the cardiac atrial natriuretic factor (ANF) promoter_the only known target for Nkx2-5. Co-expression of GATA-4 and Nkx2-5 resulted in synergistic activation of the ANF promoter in heterologous cells. The synergy involves physical Nkx2-5-GATA-4 interaction, seen in vitro and in vivo, which maps to the C-terminal zinc finger of GATA-4 and a C-terminus extension; similarly, a C-terminally extended homeodomain of Nkx2-5 is required for GATA-4 binding. Structure/function studies suggest that binding of GATA-4 to the C-terminus autorepressive domain of Nkx2-5 may induce a conformational change that unmasks Nkx2-5 activation domains. GATA-6 cannot substitute for GATA-4 for interaction with Nkx2-5. This interaction may impart functional specificity to GATA factors and provide cooperative crosstalk between two pathways critical for early cardiogenesis. Given the co-expression of GATA proteins and NK2 class members in other tissues, the GATA/Nkx partnership may represent a paradigm for transcription factor interaction during organogenesis.

Animals↗
PubMed1995

Mechanisms of autoimmune disease in the testis and ovary.

This article reviews recent research on autoimmune diseases of the testis and ovary based on two experimental approaches for induction of autoimmune diseases of the gonads (immunization with testis or ovary antigen, usually with adjuvant, and deliberate alteration of the immune system in normal animals, without injecting antigen or adjuvant). It has been found that the local testicular immunoregulatory environment partially impedes autoimmune responses to ontogenic testis antigens and regulatory T cells usually control pathogenic T cells that are found in the normal peripheral immune system. If the clonal balance of these CD4+ T cell subsets is tipped in favour of pathogenic T cells, autoimmune diseases of the gonads could ensue. Loss of regulatory T cells may occur through aberrant T cell development, or oophoritogenic T cells can be activated by non-ovarian peptides that crossreact with self peptides at the level of the T cell receptor. The inflammatory CD4 (Th1) T cell mechanism has been established to be a critical pathway for autoimmune orchitis and autoimmune oophoritis; tumour necrosis factor has been shown to be required for amplification of the pathogenic T cell response. Histopathology has suggested tissue locations wherein pathogenic T cells encounter testicular and ovarian target antigens. Antibodies bind to both testicular and ovarian target antigens during the development of autoimmune orchitis and autoimmune oophoritis, but the precise role of the antibodies has not been determined. Resolution of this role may influence the clarification of the mechanism whereby autoantibody may access ejaculated human spermatozoa to cause infertility and the future of contraceptive vaccine development based on ovarian antigens. A novel mechanism of autoantibody induction and an immunogenetic approach to autoimmune oophoritis and orchitis, based on molecular linkage analysis of inbred mice, are also reviewed.

Animals↗
PubMed2003

Antagonism of hypervitaminosis A-induced anterior neural tube closure defects with a methyl-donor deficiency in murine whole-embryo culture.

The interaction of a dietary excess of vitamin A (retinoid) and deficiency of methyl-donor compounds was examined in murine early-organogenesis embryonic development. Female mice were fed one of six diets from the time of vaginal plug detection until gestational d 8.0, when embryos were removed and grown in whole embryo culture for 46 h, using serum from rats fed the same diet for 36 d as the culture medium. The six diets were either methyl-donor deficient (designated -FCM: devoid of folic acid, choline and supplemental L-methionine, but having methionine as a component of the protein portion of the diet) or methyl-donor sufficient (designated +FCM: containing folic acid, choline and L-methionine supplementation), in combination with one of three concentrations of retinyl palmitate (0.016, 0.416 or 4.016 g/kg diet). The high dose of retinyl palmitate induced a failure of anterior neuropore closure and hypoplasia of the visceral arches, both of which were significantly ameliorated by simultaneous administration of the methyl-donor-deficient diet. The primary acidic retinoid detected in the rat serum was 9,13-di-cis-retinoic acid, although we hypothesize that teratogenic retinoids were formed by embryonic biotransformation of the retinyl esters to toxic metabolites. Biochemical measurements of metabolites in relevant pathways were performed. We propose that the amelioration of these malformations may be used to determine biochemical pathways critical for retinoid teratogenesis.

Animals↗
PubMed2001

Levels of hypoxia-inducible factor-1 alpha during breast carcinogenesis.

BACKGROUND: Hypoxia-inducible factor-1 (HIF-1) is a transcription factor that regulates gene expression in critical pathways involved in tumor growth and metastases. In this report, we investigated whether the level of HIF-1 alpha is increased during carcinogenesis in breast tissue and is associated with other tumor biomarkers. METHODS: Paraffin-embedded clinical specimens from five pathologic stages of breast tumorigenesis and from normal breast tissue were used. HIF-1 alpha protein and the biomarkers vascular endothelial growth factor (VEGF), HER-2/neu, p53, Ki-67, and estrogen receptor (ER) were identified immunohistochemically, and microvessel density (a measure of angiogenesis) was determined. Associations among levels of HIF-1 alpha and these biomarkers were tested statistically. All statistical tests are two-sided. RESULTS: The frequency of HIF-1 alpha-positive cells in a specimen increased with the specimen's pathologic stage (P<.001, chi(2) test for trend) as follows: normal breast tissue (0 specimens with > or = 1% HIF-1 alpha-positive cells in 10 specimens tested), ductal hyperplastic lesions (0 in 10), well-differentiated ductal carcinomas in situ (DCIS) (11 in 20), well-differentiated invasive breast cancers (12 in 20), poorly differentiated DCIS (17 in 20), and poorly differentiated invasive carcinomas (20 in 20). Increased levels of HIF-1 alpha were statistically significantly associated with high proliferation and increased expression of VEGF and ER proteins. In DCIS lesions, increased levels of HIF-1 alpha were statistically significantly associated with increased microvessel density. HIF-1alpha showed a borderline association with HER-2/neu but no association with p53. CONCLUSIONS: The level of HIF-1 alpha increases as the pathologic stage increases and is higher in poorly differentiated lesions than in the corresponding type of well-differentiated lesions. Increased levels of HIF-1 alpha are associated with increased proliferation and increased expression of ER and VEGF. Thus, increased levels of HIF-1 alpha are potentially associated with more aggressive tumors.

Biomarkers, Tumor↗
PubMed2000

Brief report: effects of pediatric HIV infection on mental and psychomotor development.

OBJECTIVE: To examine the effect of HIV status on infants' mental and psychomotor functioning, controlling for confounding factors such as prenatal drug exposure and birth conditions. METHODS: Twenty HIV-infected and 25 seroreverted infants (ages 3-30 months old) were administered the Bayley Scales of Infant Development (BSID) and a neurological examination at two time points, 4 to 12 months apart. The majority were from ethnic minority, socioeconomically disadvantaged families; 67% of the infants were prenatally drug-exposed. RESULTS: HIV-infected infants had significantly lower scores on the BSID at baseline (mental development) and follow-up (motor development) compared to seroreverters. When HIV and neurological deficits were considered together, HIV+ children with neurological deficits scored significantly lower than HIV+ children without neurological deficits and seroreverters, with and without neurological diagnoses. Prenatal drug exposure was not associated with performance on the BSID. CONCLUSIONS: These data suggest that CNS involvement is a critical pathway by which HIV affects infants' neurodevelopment.

Analysis of Variance↗
PubMed2002

Amelioration of ozone-induced lung injury by anti-tumor necrosis factor-alpha.

Ozone (O(3)) is a significant component of atmospheric air pollution and produces detrimental effects in the lung. Although the mechanism of O(3)-induced lung inflammation and injury is unclear, the increased release of the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) by lung cells following O(3) exposure may shed some light on this subject. To investigate the role of TNF-alpha in the O(3)-induced pulmonary insult, we intraperitoneally injected rats with either rabbit preimmune serum or rabbit antirat TNF-alpha 1 h prior to O(3) exposure. Approximately 12 h after the end of O(3) exposure the animals were sacrificed, the lungs lavaged, and tissue samples collected for expression of cytokine genes relevant to inflammation. The bronchoalveolar lavage fluid (BALF) was analyzed for albumin as a marker of pulmonary epithelial permeability changes and for fibronectin for its role in lung injury and repair. The lavage cells were collected, counted, and identified to quantitate the inflammatory response. Ozone exposure resulted in a significant increase in BALF albumin and fibronectin as compared to air-exposed controls and a significant increase in BALF polymorphonuclear leukocytes (PMNs). Antibody treatment produced a significant decrease in BALF albumin and PMNs as compared to O(3)-exposed rats given preimmune serum. Antibody treatment did not affect the BALF fibronectin concentration or the total cell count in the BAL. Tissue analysis for gene arrays revealed an activation of IL-1alpha, IL-6, and IL-10 in animals exposed to O(3). The gene expression was downregulated in animals treated with anti-TNF-alpha antibody prior to O(3) exposure. The results suggest a central role for TNF-alpha in the mechanistic pathways critical to lung inflammation. The significance of TNF-alpha in the inflammation and epithelial injury produced by ozone exposure reflects its overall contribution through modulation of other cytokines.

Albumins↗
PubMed2001

Gene expression profiles of proliferating vs. G1/G0 arrested human leukemia cells suggest a mechanism for glucocorticoid-induced apoptosis.

Glucocorticoids (GC) have pronounced effects on metabolism, differentiation, proliferation, and cell survival (1). In certain lymphocytes and lymphocyte-related malignancies, GC inhibit proliferation and induce apoptotic cell death, which has led to their extensive use in the therapy of malignant lymphoproliferative disorders (2). Most of these effects result from regulation of gene expression via the GC receptor (GR), a ligand-activated transcription factor (3). Although hundreds of genes are regulated by GC (1), how certain biological GC effects relate to individual gene regulation remains enigmatic. To address this question with respect to GC-induced cell cycle arrest and apoptosis, we applied DNA chip technology (4, 5) to determine gene expression profiles in proliferating and G1/G0-arrested (by conditional expression of the CDK inhibitor p16/INK4a) acute lymphoblastic T cells undergoing GC-induced apoptosis. Of 7074 genes tested, 163 were found to be regulated by dexamethasone in the first 8 h in proliferating cells and 66 genes in G1/G0-arrested cells. An almost nonoverlapping set of genes (i.e., only eight genes) was coordinately regulated in proliferating and arrested cells. Analysis of the regulated genes supports the concept that GC-induced apoptosis results from positive GR autoregulation entailing persistent down-regulation of metabolic pathways critical for survival

Apoptosis↗
PubMed1998

Current therapy of the patent ductus arteriosus.

The patent ductus arteriosus (PDA) was the first congenital heart lesion to be treated surgically and also the first to be treated with nonsurgical catheter intervention. Surgical ligation and division of the ductus remains the gold standard for consistently achieving complete occlusion. Transaxillary muscle-sparing thoracotomy and video-assisted thoracoscopic ligation, however, have evolved as surgical alternatives with reduced trauma, shorter hospitalization, and excellent cosmetic result but are associated with a significant rate of residual or recurrent duct patency. With aggressive application of critical pathway methods, significant reduction in cost has been achieved for surgical PDA closure. Nonsurgical transcatheter closure nevertheless has gained widespread acceptance, mostly employing detachable or nondetachable stainless steel coils. Coils have superseded the previously popular Rashkind PDA occluder (USCI/Bard, Tewksbury, MA) because of significantly lower cost, less cumbersome handling, smaller delivery catheters, and superior occlusion rates. Various coil implantation techniques and detachment mechanisms have been devised. Large PDAs with smallest diameter greater than 5 mm, however, still are better treated surgically until appropriate devices become available.

Age Factors↗
PubMed1997

Variance analysis for care path outcomes management.

Variance analysis and monitoring procedures of clinical care path interventions and outcomes are discussed with the objective of modifying suboptimal care paths into optimal pathways. These critical care paths will contain value-added interventions that contribute significantly to the achievement of measurable outcomes. Care path variables are defined and measurement considerations are presented. Variance analysis procedures, measures, and uses are discussed that facilitate outcomes management and continuous quality improvement.

Analysis of Variance↗
PubMed1985

Food-chain transfer of U-series radionuclides in a northern Saskatchewan aquatic system.

Levels of TotalU, 226Ra, and 210Pb in water, sediments, insects and fish were measured in a stream and a lake affected by U mill effluents and in three uncontaminated systems (one creek and two lakes). Radionuclide levels were significantly elevated in water, sediments and biota at contaminated sites. Radionuclide concentration declined with each successive trophic level due primarily to very low assimilation efficiency. Fish radionuclide concentrations varied with season but did not vary with age or year of sampling. Distribution coefficients were high; therefore, a large proportion of radionuclides entering the systems go to the solid phase. Organisms feeding on or near sediments had higher radionuclide levels than pelagic species. There is a potential for long-term cycling of radionuclides from sediments through food chains due to low flux and sedimentation rates. With the exception of water----insects and water----fish all transfer coefficients (TC) were low, usually less than one. Control TCs were greater than TCs in contaminated areas. Radium-226 and 210Pb TCs declined dramatically at the insect-fish level. Uranium uptake from water by insects and fish was much less than 226Ra or 210Pb uptake. Uptake from sediments was similar for all nuclides in insects but 210Pb sediment-fish TCs differed from 226Ra or U TCs. The critical pathway in the contaminated area was sediments----insects----forage fish----whitefish----man. Estimated internal dose rates to large fish in the contaminated area were 1-2 rad/y. Dose to humans from consumption of one fish serving per week for 1 y was 2% of the International Commission on Radiological Protection (ICRP) annual limit for the general public.

Animals↗
PubMedDate not supplied

Treatment of pain in acutely burned children.

The child with burns suffers severe pain at the time of the burn and during subsequent treatment and rehabilitation. Pain has adverse physiological and emotional effects, and research suggests that pain management is an important factor in better outcomes. There is increasing understanding of the private experience of pain, and how children benefit from honest preparation for procedures. Developmentally appropriate and culturally sensitive pain assessment, pain relief, and reevaluation have improved, becoming essential in treatment. Pharmacological treatment is primary, strengthened by new concepts from neurobiology, clinical science, and the introduction of more effective drugs with fewer adverse side effects and less toxicity. Empirical evaluation of various hypnotic, cognitive, behavioral, and sensory treatment methods is advancing. Multidisciplinary assessment helps to integrate psychological and pharmacological pain-relieving interventions to reduce emotional and mental stress, and family stress as well. Optimal care encourages burn teams to integrate pain guidelines into protocols and critical pathways for improved care.

Analgesia, Patient-Controlled↗
PubMed1998

Factors influencing selected lengths of ICU stay for coronary artery bypass patients.

This study examines factors influencing the length of intensive care unit stay for patients after coronary artery bypass surgery. Profiles of patients with selected lengths of ICU stay were identified for Group 1 (< or =1 day) and Group 2 (> or =2 days). Medical records of 175 patients who had undergone this procedure at an urban teaching hospital were reviewed. Patients who had a 1-day ICU length of stay were younger (mean=62.39, SD=10.88) and had comorbidities such as hypertension. Those patients with an ICU length of stay 2 days or longer were older (mean=68.18, SD=11.84) and had preoperative comorbidities such as congestive heart failure, chronic obstructive pulmonary disease, ejection fraction <50%, and need for an intra-aortic balloon pump. Atrial dysrhythmias, low cardiac output syndrome, renal insufficiency, and respiratory insufficiency were the postoperative complications associated with a prolonged ICU length of stay. Knowledge of the factors influencing selected lengths of ICU stay will enable nurses to choose patients for critical pathways and to anticipate postoperative problems in high-risk patients.

Adult↗
PubMed1996

Mobility in older patients with hip fractures: examining prefracture status, complications, and outcomes at discharge from the acute-care hospital.

The purpose of this study was to examine the relationships among prefracture status, development of complications, mobility outcomes at discharge, and disposition at discharge. We singled out a case series of consecutive noninstitutionalized elderly persons hospitalized for hip fracture (ICD 820.0-820.9) at two Baltimore hospitals during 1992-1993. Data were abstracted from the medical records for the following variables: sociodemographic information, prefracture status, selected medical conditions, injury and surgical treatment, complications, functional mobility and assistance needed at discharge, and disposition. Factors associated with four complications were identified from multiple logistic regression analyses. (a) Prefracture needs for assistance with activities of daily living (ADL), and age > or = 80, were associated with the development of pressure ulcers. (b) Male gender and prefracture urinary incontinence (UI) were associated with pneumonia. (c) Prefracture UI and weight-bearing status were associated with UI after removal of an indwelling catheter. (d) Age > or = 80 was associated with urinary retention. The amount of assistance needed for mobility tasks at discharge was associated with prefracture need for assistance with ADLs, gender, weight-bearing status, and hospitals with shorter lengths of stay and fewer physical therapy sessions. Patients who were older and had shorter lengths of stay and less physical therapy were more likely to go to another health facility than directly home. Prefracture status (ADL, prefracture UI) was significantly associated with the development of complications. Prefracture needs for assistance with ADL and complications were associated with mobility outcomes at discharge. These prefracture factors have an effect on outcomes and need to be addressed in the development of critical pathways for case treatment. Specific protocols for subgroups of patients may need to be designed and evaluated.

Activities of Daily Living↗