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Biomedical subjects

David Ross

Publications and source records attributed to David Ross.

At least 19 recordsLinked to original sources

Gradient elution moving boundary electrophoresis for high-throughput multiplexed microfluidic devices.

A novel method for performing electrophoretic separations is described-gradient elution moving boundary electrophoresis (GEMBE). The technique utilizes the electrophoretic migration of chemical species in combination with variable hydrodynamic bulk counterflow of the solution through a separation capillary or microfluidic channel. Continuous sample introduction is used, eliminating the need for a sample injection mechanism. Only analytes with an electrophoretic velocity greater than the counterflow velocity enter the separation channel. The counterflow velocity is varied over time so that each analyte is brought into the separation column at different times, allowing for high-resolution separations in very short channels. The new variable of bulk flow acceleration affords a new selectivity parameter to electrophoresis analogous to gradient elution compositions in chromatography. Because it does not require extra channels or access ports to form an injection zone and because separations can be performed in very short channels, GEMBE separations can be implemented in much smaller areas on a micro-fluidic chip as compared to conventional capillary electrophoresis. Demonstrations of GEMBE separations of small dye molecules, amino acids, DNA, and immunoassay products are presented. A low-cost, polymeric, eight-channel multiplexed microfluidic device was fabricated to demonstrate the reduced area requirements of GEMBE; the device was less than 1 in.2 in area and required only n + 1 fluidic access ports per n analyses (in this instance, nine ports for eight analyses). Parallel separations of fluorescein and carboxyfluorescein yielded less than 3% relative standard deviation (RSD) in interchannel migration times and less than 5% RSD in both peak and height measurements. The device was also used to generate a calibration curve for a homogeneous insulin immunoassay using each of the eight channels as a calibration point with less than 5% RSD at each point with replicate analyses.

Journal Article↗

Enzyme specific activation of benzoquinone ansamycin prodrugs using HuCC49DeltaCH2-beta-galactosidase conjugates.

To activate prodrugs for cancer treatment, an anti-TAG-72 antibody (HuCC49DeltaCH2) was used for delivery of an activation enzyme (beta-galactosidase) to specifically activate a geldanamycin prodrug (17-AG-C2-Gal) against colon cancer. The geldanamycin prodrug 17-AG-C2-Gal was synthesized by coupling a galactose-amine derivative with geldanamycin at the C-17 position. Molecular docking with two different programs (Affinity and Autodock) showed that the prodrug (17-AG-C2-Gal) was unable to bind to Hsp90; however, the product (17-AG-C2), enzymatically cleaved by beta-galactosidase conjugate, bound to Hsp90 in a similar way as geldanamycin and 17-AG. The computational docking results were further confirmed in experimental testing by the tetrazolium [3-(4,5-dimethythiazol-2-yl)]-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium assay and mass spectrometry. HuCC49DeltaCH2 was chemically conjugated to beta-galactosidase. The antibody-enzyme conjugate was able to target tumor antigen TAG-72 with the well-preserved enzymatic activity to activate 17-AG-C2-Gal prodrug. The released active drug 17-AG-C2 was demonstrated to induce up to 70% AKT degradation and enhance anticancer activity by more than 25-fold compared to the prodrug.

Antibodies, Monoclonal↗

Scanning temperature gradient focusing.

Temperature gradient focusing (TGF) is a recently developed technique for the simultaneous concentration and electrophoretic separation of ionic analytes in microfluidic channels. One drawback to TGF as it has previously been described is the limited peak capacity; only a small number of analyte peaks (approximately 2-3) can be simultaneously focused and separated. In this paper, we report on a variation of the TGF method whereby the bulk flow rate is varied over time so that a large number of analytes can be sequentially focused, moved past a fixed detection point, and flushed to waste. In addition to improved peak capacity, the detection limits of the scanning TGF method can be adjusted on-the-fly, as needed for different samples. Finally, scanning TGF provides a technique by which high-resolution, high-peak-capacity electrophoretic separations can be performed in simple, straight, and short microfluidic channels.

Journal Article↗

The bioreduction of a series of benzoquinone ansamycins by NAD(P)H:quinone oxidoreductase 1 to more potent heat shock protein 90 inhibitors, the hydroquinone ansamycins.

We have previously evaluated the role of NAD(P)H:quinone oxidoreductase 1 (NQO1) in the bioreductive metabolism of 17-(allylamino)-demethoxygeldanamycin (17AAG) to the corresponding hydroquinone, a more potent 90-kDa heat shock protein (Hsp90) inhibitor. Here, we report an extensive study with a series of benzoquinone ansamycins, which includes gel-danamycin, 17-(amino)-17-demethoxygeldanamycin, and 17-demethoxy-17-[[2-(dimethylamino)ethyl]amino]-geldanamycin. The reduction of these benzoquinone ansamycins by recombinant human NQO1 to the corresponding hydroquinone ansamycins was monitored by high-performance liquid chromatography (HPLC) and confirmed by liquid chromatography/mass spectrometry. Inhibition of purified yeast Hsp90 ATPase activity was augmented in the presence of NQO1 and abrogated by 5-methoxy-1,2-dimethyl-3-[(4-nitrophenoxy)methyl-]indole-4,7-dione (ES936), a mechanism-based inhibitor of NQO1, showing that the hydroquinone ansamycins were more potent Hsp90 inhibitors than their parent quinones. An isogenic pair of human breast cancer cell lines, MDA468 and MDA468/NQ16, differing in expression of NQO1, was used, and HPLC analysis showed that hydroquinone ansamycins were formed by the MDA468/NQ16 cells, which could be prevented by ES936 pretreatment. The MDA468/NQ16 cells were more sensitive to growth inhibition after treatment with the benzoquinone ansamycins compared with the MDA468 cells; this increased sensitivity could be reduced by ES936 pretreatment. The increased duration of benzoquinone ansamycin exposure showed increased potency and -fold inhibition in MDA468/NQ16 cells relative to the parental MDA468 cells. Computational-based molecular modeling studies displayed additional contacts between yeast Hsp90 and the hydroquinone ansamycins, which translated to greater interaction energies compared with the corresponding benzoquinone ansamycins. In conclusion, these studies show that the reduction of this series of benzoquinone ansamycins by NQO1 generates the corresponding hydroquinone ansamycins, which exhibit enhanced Hsp90 inhibition.

Benzoquinones↗

A potential role for cyclized quinones derived from dopamine, DOPA, and 3,4-dihydroxyphenylacetic acid in proteasomal inhibition.

We examined the ability of oxidation products of dopamine, DOPA, and 3,4-dihydroxyphenylacetic acid (DOPAC) to inhibit proteasomal activity. Dopamine, DOPA, and DOPAC underwent tyrosinase-catalyzed oxidation to generate aminochrome, dopachrome, and furanoquinone, respectively. In these studies, the oxidation of dopamine by tyrosinase generated product(s) that inhibited the proteasome, and proteasomal inhibition correlated with the presence of the UV-visible spectrum of aminochrome. The addition of superoxide dismutase and catalase did not prevent proteasomal inhibition. The addition of NADH and the quinone reductase NAD(P)H:quinone oxidoreductase 1 (NQO1) protected against aminochrome-induced proteasome inhibition. Although NQO1 protected against dopamine-induced proteasomal inhibition, the metabolism of aminochrome by NQO1 led to oxygen uptake because of the generation of a redox-labile cyclized hydroquinone, further demonstrating the lack of involvement of oxygen radicals in proteasomal inhibition. DOPA underwent tyrosinase-catalyzed oxidation to form dopachrome, and similar to aminochrome, proteasomal inhibition correlated with the presence of a dopachrome UV-visible spectrum. The inclusion of NQO1 did not protect against proteasomal inhibition induced by dopachrome. Oxidation of DOPAC by tyrosinase generated furanoquinone, which was a poor proteasome inhibitor. These studies demonstrate that oxidation products, including cyclized quinones derived from dopamine and related compounds, rather than oxygen radicals have the ability to inhibit the proteasome. They also suggest an important protective role for NQO1 in protecting against dopamine-induced proteasomal inhibition. The ability of endogenous intermediates formed during dopaminergic metabolism to cause proteasomal inhibition provides a potential basis for the selectivity of dopaminergic neuron damage in Parkinson's disease.

3,4-Dihydroxyphenylacetic Acid↗

Nrf2 controls bone marrow stromal cell susceptibility to oxidative and electrophilic stress.

Understanding the molecular pathway(s) controlling the expression of stromal cellular antioxidants and phase 2 enzymes is of importance for developing strategies to protect against bone marrow toxicity induced by oxidants and electrophiles. Accordingly, this study was undertaken to determine the role of the nuclear factor E2-related factor 2 (Nrf2) in regulation of both constitutive and chemoprotectant-inducible expression of antioxidants and phase 2 enzymes in mouse bone marrow stromal cells. The constitutive expression of a series of antioxidants and phase 2 enzymes was significantly lower in stromal cells derived from Nrf2 knockout (Nrf2(-/-)) mice than those from wild-type littermates (Nrf2(+/+)). Incubation of Nrf2(+/+) stromal cells with 3H-1,2-dithiole-3-thione (D3T) led to a significant induction of various antioxidants and phase 2 enzymes. The inducibility of the above cellular defenses by D3T was abolished in Nrf2(-/-) cells. As compared to wild-type cells, Nrf2(-/-) cells were much more susceptible to cytotoxicity induced by reactive oxygen or nitrogen species, 4-hydroxy-2-nonenal, 1,4-hydroquinone, or 1,4-benzoquinone. Upregulation of the antioxidants and phase 2 enzymes by D3T in Nrf2(+/+) stromal cells resulted in increased resistance to the above oxidant- and electrophile-induced cytotoxicity, whereas D3T treatment of Nrf2(-/-) cells only provided a marginal cytoprotection. Taken together, this study demonstrates that Nrf2 is crucial in controlling the expression of bone marrow stromal antioxidants and phase 2 enzymes as well as the susceptibility of these cells to oxidative and electrophilic stress.

Animals↗

Identification of two gene variants associated with risk of advanced fibrosis in patients with chronic hepatitis C.

BACKGROUND & AIMS: Previously identified clinical risk factors such as sex, alcohol consumption, and age at infection do not accurately predict which patients with chronic hepatitis C (CHC) will develop advanced fibrosis (bridging fibrosis and cirrhosis). The aim of this study was to identify genetic polymorphisms that can predict the risk of advanced fibrosis in patients with CHC. METHODS: A total of 916 subjects with CHC was enrolled from 2 centers. A gene-centric disease association study of 24,832 putative functional, single nucleotide polymorphisms (SNPs) was performed. Of the 1609 SNPs that were significantly associated (P </= .05) with advanced fibrosis in the discovery cohort (University of California San Francisco [UCSF], N = 433), the first batch of 100 SNPs were selected for validation in the replication cohort (Virginia Commonwealth University [VCU], N = 483). RESULTS: A missense SNP in the DEAD box polypeptide 5 (DDX5) gene was significantly associated with an increased risk of advanced fibrosis in both the UCSF and the VCU cohorts (OR, 1.8 and 2.2, respectively). Two diplotype groups, carrying the haplotypes composed of the DDX5 SNP and 2 neighboring POLG2 SNPs were also significantly associated with an increased risk of advanced fibrosis and had comparable or better risk estimates. In addition, a missense SNP in the carnitine palmitoyltransferase 1A (CPT1A) gene was associated with a decreased risk of advanced fibrosis in both the UCSF and the VCU cohorts (OR, 0.3 and 0.6, respectively). CONCLUSIONS: Subjects with CHC carrying DDX5 minor allele or DDX5-POLG2 haplotypes are at an increased risk of developing advanced fibrosis, whereas those carrying the CPT1A minor allele are at a decreased risk.

Adolescent↗

Quantitative temperature gradient focusing performed using background electrolytes at various pH values.

Temperature gradient focusing (TGF) has previously been shown to be a practical technique for simultaneous concentration and separation of a variety of samples. In this paper, we demonstrate that TGF can be conducted at a wide range of pH values. Techniques for first-order prediction of the suitability of a given BGE for focusing are discussed. Buffer suitability for TGF is assessed experimentally by simultaneously concentrating and separating a pair of fluorescent analytes. One analyte is held at constant concentration for use as an internal standard while the concentration of the other dye is varied. Peak area is shown to vary linearly with the input dye concentration. A high degree of resolution (R(s) >3) of fluorescein and carboxyfluorescein, as well as for two LysoSensor-based dyes, is also observed. Foucusing and separation by TGF was successfully conducted quantitatively in BGE solutions of pH from 3.0 to 10.5.

Buffers↗

Mycobacterium ulcerans ulcers: a proposed surgical management algorithm.

Mycobacterium ulcerans (MU) is the third common mycobacterial infection after tuberculosis and leprosy. In endemic areas, MU ulcers should be considered in the differential diagnosis of any unusual or nonhealing lesion or ulcer. Diagnosis and treatment should be instigated promptly. Delay may lead to disfiguring or disabling scars. Surgical management, therefore, should aim towards early excision, with clear margins of the ulcer. We present 4 consecutive patients treated by our department within a 6-month period for MU ulcers. The presentation, diagnosis and surgical management are described. Based on our experience and after reviewing the literature, we have developed a surgical algorithm for the management of MU ulcers.

Algorithms↗

5-Methoxy-1,2-dimethyl-3-[(4-nitrophenoxy)methyl]indole-4,7-dione, a mechanism-based inhibitor of NAD(P)H:quinone oxidoreductase 1, exhibits activity against human pancreatic cancer in vitro and in vivo.

The enzyme NAD(P)H:quinone oxidoreductase 1 (NQO1) has been found to be up-regulated in pancreatic cancer as well as many other solid tumors. A recent study showed that inhibition of NQO1 in pancreatic cancer cells using the nonselective inhibitor dicumarol suppressed the malignant phenotype. The authors suggested that inhibition of cell growth might result from an increase in intracellular superoxide production due to inhibition of NQO1. We have recently shown that NQO1 can directly scavenge superoxide and this effect may become physiologically relevant in cells containing high NQO1 levels. We therefore tested the hypothesis that 5-methoxy-1,2-dimethyl-3-[(4-nitrophenoxy)methyl]indole-4,7-dione (ES936), a specific mechanism-based inhibitor of NQO1, would be an effective agent for the treatment of pancreatic tumors. The human pancreatic tumor cell lines BxPC-3 and MIA PaCa-2 contain high levels of NQO1 activity and protein as verified by immunoblot and immunocytochemical staining of human pancreatic tumor cells. ES936 treatment inhibited NQO1 activity by >98% in MIA PaCa-2 and BxPC-3 cells. In addition, ES936 treatment induced growth inhibition [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay] in MIA PaCa-2 and BxPC-3 cells with an IC(50) of 108 and 365 nmol/L, respectively. Treatment of MIA PaCa-2 cells with ES936 also inhibited the ability of these cells to form colonies and grow in soft agar in a dose-dependent manner. Treatment of mice carrying MIA PaCa-2 xenograft tumors with ES936 resulted in a significant difference in growth rates in ES936-treated and DMSO-treated (control) tumors. Our data did not show an increase in either intracellular superoxide production or oxygen consumption after treatment of cells with ES936, contrary to the effects seen with dicumarol. In summary, mechanism-based inhibitors of NQO1, such as ES936, may be useful therapeutic agents for the treatment of pancreatic cancer, although the underlying mechanism seems to be independent of superoxide generation.

Animals↗

Update of the NAD(P)H:quinone oxidoreductase (NQO) gene family.

The NAD(P)H:quinone acceptor oxidoreductase (NQO) gene family belongs to the flavoprotein clan and, in the human genome, consists of two genes (NQO1 and NQO2). These two genes encode cytosolic flavoenzymes that catalyse the beneficial two-electron reduction of quinones to hydroquinones. This reaction prevents the unwanted one-electron reduction of quinones by other quinone reductases; one-electron reduction results in the formation of reactive oxygen species, generated by redox cycling of semiquinones in the presence of molecular oxygen. Both the mammalian NQO1 and NQO2 genes are upregulated as a part of the oxidative stress response and are inexplicably overexpressed in particular types of tumours. A non-synonymous mutation in the NQO1 gene, leading to absence of enzyme activity, has been associated with an increased risk of myeloid leukaemia and other types of blood dyscrasia in workers exposed to benzene. NQO2 has a melatonin-binding site, which may explain the anti-oxidant role of melatonin. An ancient NQO3 subfamily exists in eubacteria and the authors suggest that there should be additional divisions of the NQO family to include the NQO4 subfamily in fungi and NQO5 subfamily in archaebacteria. Interestingly, no NQO genes could be identified in the worm, fly, sea squirt or plants; because these taxa carry quinone reductases capable of one- and two-electron reductions, there has been either convergent evolution or redundancy to account for the appearance of these enzyme functions whenever they have been needed during evolution.

Animals↗

Paediatric transverse divergent dislocation of the elbow.

Paediatric elbow dislocations are uncommon injuries, accounting for 3-6% of all elbow injuries in childhood. A divergent elbow dislocation is an even more infrequent injury, where in addition to the elbow dislocation there is divergence of the proximal radius and ulna, either in a transverse (extremely rare) or in an anteroposterior plane, as a result of the distal humerus being forced between the proximal ends of the forearm bones. The lesion results from indirect forces transmitted to the elbow from a fall on the outstretched hand. The authors report a case of transverse divergent elbow dislocation in an 8-year-old boy, treated by closed reduction and immobilisation in a cast. At 6 months follow-up the patient had regained a full range of motion, without instability or pain.

Child↗

Risk factors influencing HIV infection incidence in a rural African population: a nested case-control study.

BACKGROUND: Risk factors influencing the incidence of human immunodeficiency virus (HIV) infection were investigated in a case-control study nested within a community-randomized trial of treatment of syndromic sexually transmitted infections (STIs) in rural Tanzania. METHODS: Case patients were persons who became HIV positive, and control subjects were randomly selected from among persons who remained HIV negative. For each sex, we obtained adjusted odds ratios (ORs) and population-attributable fractions (PAFs) for biomedical and behavioral factors. RESULTS: We analyzed 92 case patients and 903 control subjects. In both sexes, the incidence of HIV infection was significantly higher in subjects with an HIV-positive spouse than in those with HIV-negative spouse (men: OR, 25.1; women: OR, 34.0). The incidence of HIV infection was significantly higher in those who became positive for herpes simplex virus type 2 (HSV-2) (men: OR, 5.60; women: OR, 4.76) and those who were HSV-2-positive at baseline (men: OR, 3.66; women: OR, 2.88) than in subjects who were HSV-2 negative. In women, living elsewhere (OR, 3.22) and never having given birth (OR, 4.27) were significant risk factors. After adjustment, the incidence of HIV infection was not significantly associated with a history of injections or STIs in either sex. CONCLUSION: HSV-2 infection was the most important risk factor for HIV infection, which highlights the need for HSV-2 interventions in HIV infection control, and there were particularly strong associations with recent HSV-2 seroconversion. The PAF associated with having an HIV-positive spouse was low, but this is likely to increase during the epidemic.

Adolescent↗

Formation of 17-allylamino-demethoxygeldanamycin (17-AAG) hydroquinone by NAD(P)H:quinone oxidoreductase 1: role of 17-AAG hydroquinone in heat shock protein 90 inhibition.

We have examined the role of NAD(P)H:quinone oxidoreductase 1 (NQO1) in the bioreductive metabolism of 17-allylamino-demethoxygeldanamycin (17-AAG). High-performance liquid chromatography (HPLC) analysis of the metabolism of 17-AAG by recombinant human NQO1 revealed the formation of a more polar metabolite 17-AAGH2. The formation of 17-AAGH2 was NQO1 dependent, and its formation could be inhibited by the addition of 5-methoxy-1,2-dimethyl-3-[(4-nitrophenoxy)methyl]indole-4,7-dione (ES936), a mechanism-based (suicide) inhibitor of NQO1. The reduction of 17-AAG to the corresponding hydroquinone 17-AAGH2 was confirmed by tandem liquid chromatography-mass spectrometry. 17-AAGH2 was relatively stable and only slowly underwent autooxidation back to 17-AAG over a period of hours. To examine the role of NQO1 in 17-AAG metabolism in cells, we used an isogenic pair of human breast cancer cell lines differing only in NQO1 levels. MDA468 cells lack NQO1 due to a genetic polymorphism, and MDA468/NQ16 cells are a stably transfected clone that express high levels of NQO1 protein. HPLC analysis of 17-AAG metabolism using cell sonicates and intact cells showed that 17-AAGH2 was formed by MDA468/NQ16 cells, and formation of 17-AAGH2 could be inhibited by ES936. No 17-AAGH2 was detected in sonicates or intact MDA468 cells. Following a 4-hour treatment with 17-AAG, the MDA468/NQ16 cells were 12-fold more sensitive to growth inhibition compared with MDA468 cells. More importantly, the increased sensitivity of MDA468/NQ16 cells to 17-AAG could be abolished if the cells were pretreated with ES936. Cellular markers of heat shock protein (Hsp) 90 inhibition, Hsp70 induction, and Raf-1 degradation were measured by immunoblot analysis. Marked Hsp70 induction and Raf-1 degradation was observed in MDA468/NQ16 cells but not in MDA468 cells. Similarly, downstream Raf-1 signaling molecules mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) kinase and ERK also showed decreased levels of phosphorylation in MDA468/NQ16 cells but not in MDA468 cells. The ability of 17-AAG and 17-AAGH2 to inhibit purified yeast and human Hsp90 ATPase activity was examined. Maximal 17-AAG-induced ATPase inhibition was observed in the presence of NQO1 and could be abrogated by ES936, showing that 17-AAGH2 was a more potent Hsp90 inhibitor compared with 17-AAG. Molecular modeling studies also showed that due to increased hydrogen bonding between the hydroquinone and the Hsp90 protein, 17-AAGH2 was bound more tightly to the ATP-binding site in both yeast and human Hsp90 models. In conclusion, these studies have shown that reduction of 17-AAG by NQO1 generates 17-AAGH2, a relatively stable hydroquinone that exhibits superior Hsp90 inhibition.

Benzoquinones↗

Clinical applications of forced oscillation to assess peripheral airway function.

Forced oscillation applies external pressures to the respiratory system to measure respiratory impedance. Impedance of larger central airways may be dissected from that of peripheral airways using multiple oscillation frequencies. Respiratory impedance is calculated by computer-assisted methods that yield separate resistive and reactive components. The reactive component includes respiratory system capacitative and inertive properties, which may be separately visualized for clinical purposes using resonance as a rough dividing line. Low oscillation frequencies comprise those below resonance, and relate most prominently to capacitative properties of peripheral airways. High oscillation frequencies comprise those greater than resonance, which relate most prominently to inertial properties of larger central airways. Measurements of resistance and reactance in patients with peripheral airway disease, before and after therapeutic intervention, manifest characteristic patterns of response in low frequency resistance and reactance measures that appear to be closely correlated with each other. In contrast, changes in large central airways manifest resistance change uniformly over low and high frequencies.

Airway Resistance↗

Outcomes in octogenarians undergoing coronary artery bypass grafting.

BACKGROUND: Although octogenarians are being referred for coronary artery bypass grafting (CABG) with increasing frequency, contemporary outcomes have not been well described. We examined data from 4 Canadian centres to determine outcomes of CABG in this age group. METHODS: Data for the years 1996 to 2001 were examined in a comparison of octogenarians with patients less than 80 years of age. Logistic regression analysis was used to adjust for preoperative factors and to generate adjusted rates of mortality and postoperative stroke. RESULTS: A total of 15,070 consecutive patients underwent isolated CABG during the study period. Overall, 725 (4.8%) were 80 years of age or older, the proportion increasing from 3.8% in 1996 to 6.2% in 2001 (p for linear trend = 0.03). The crude rate of death was higher among the octogenarians (9.2% v. 3.8%; p < 0.001), as was the rate of stroke (4.7% v. 1.6%, p < 0.001). The octogenarians had a significantly greater burden of comorbid conditions and more urgent presentation at surgery. After adjustment, the octogenarians remained at greater risk for in-hospital death (odds ratio [OR] 2.64, 95% confidence interval [CI] 1.95-3.57) and stroke (OR 3.25, 95% CI 2.15-4.93). Mortality declined over time for both age groups (p for linear trend < 0.001 for both groups), but the incidence of postoperative stroke did not change (p for linear trend = 0.61 [age < 80 years] and 0.08 [age > or = 80 years]). Octogenarians who underwent elective surgery had crude and adjusted rates of death (OR 1.31, 95% CI 0.60-2.90) and stroke (OR 1.59, 95% CI 0.57-4.44) that were higher than but not significantly different from those for non-octogenarians who underwent elective surgery. INTERPRETATION: In this study, rates of death and stroke were higher among octogenarians, although the adjusted differences in mortality over time were decreasing. The rate of adverse outcomes in association with elective surgery was similar for older and younger patients.

Age Factors↗