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M J O'Neill

Publications and source records attributed to M J O'Neill.

At least 19 recordsLinked to original sources

Nicotine, but neither the alpha4beta2 ligand RJR2403 nor an alpha7 nAChR subtype selective agonist, protects against a partial 6-hydroxydopamine lesion of the rat median forebrain bundle.

Although previous studies suggest nicotine protects against a 6-hydroxydopamine (6-OHDA)-induced lesion of the nigrostriatal tract in rats, it is not known whether functional motor recovery occurs or which nicotinic acetylcholine receptor (nAChR) subtypes mediate this effect. These issues were investigated by comparing the effects of the subtype-specific nAChR agonists, RJR2403 (alpha4beta2 preferring) and (R)-N-(1-azabicyclo[2.2.2.]oct-3-yl)(5-(2-pyridyl)thiopene-2-carboxamide (Compound A; alpha7-selective) and nicotine given 30 min prior to and daily for 14 days after a partial 6-OHDA lesion. In vehicle treated animals, 6-OHDA (6 microg) produced a 65 +/- 1.8% loss of striatal tyrosine hydroxylase (TH) immunoreactivity in the lesion versus intact hemisphere. This loss was reduced in animals treated with nicotine (0.6 and 0.8 mg kg(-1)), reaching significance at the higher dose (36.6 +/- 3.7% loss; P < 0.01 versus vehicle). Treatment with nicotine (0.6 and 0.8 mg kg(-1)) also significantly reduced the number of amphetamine-induced rotations compared to vehicle treatment. In contrast, treatment with RJR2403 (0.2 and 0.4 mg kg(-1)) or Compound A (10 and 20 mg kg(-1)) reduced neither the degree of amphetamine-induced rotations nor the loss of striatal TH immunoreactivity. These data suggest that whilst nicotine is neuroprotective in this partial lesion model, activation of neither the alpha4beta2 nor alpha7 subtypes alone is sufficient to provide protection.

Analysis of Variance↗

Prevalence and distribution of adnexal findings suggesting endometriosis in patients with MR diagnosis of adenomyosis.

The purpose of this investigation was to establish the prevalence and distribution of MR findings associated with pelvic endometriosis in patients with a MRI diagnosis of adenomyosis. Retrospective review of the pelvic MRI in 59 patients (age 32-54 years, mean 42 years) who met strict MRI criteria for adenomyosis was performed. T1 weighted fat saturated and T2 weighted images in these patients were reviewed for the presence or absence of T1 bright signal suggesting endometriosis in any of nine locations (uterine serosa, right and left ovary, right and left fallopian tube, right and left broad ligament, and right and left pelvic side wall). 20 (20/59) patients (34%), showed characteristic MRI features associated with endometriosis. A total of 54 sites of involvement were identified (uterine serosa n = 17, ovaries n = 14, broad ligaments n = 10, fallopian tubes n = 8, pelvic side walls n = 5) in 20 patients with an average of 2.7 sites per patient. Implants (n = 43) were more common than endometriomas (n = 11). Endometriomas occurred most often in the ovaries (ovaries n = 9, broad ligament n = 2) whereas implants were seen on all locations (uterine serosa n = 17, ovaries n = 5, broad ligaments n = 8, fallopian tubes n = 8, pelvic side walls n = 5). One third of patients with adenomyosis diagnosed by MRI also had MRI findings of endometriosis, with serosal implants being the most common finding. Imaging protocols should routinely include T1 weighted fat saturated imaging sequences in order to detect coexistent endometriosis in patents undergoing pelvic MRI for the diagnosis of adenomyosis.

Abdominal Wall↗

Chronic pre-treatment with nicotine enhances nicotine-evoked striatal dopamine release and alpha6 and beta3 nicotinic acetylcholine receptor subunit mRNA in the substantia nigra pars compacta of the rat.

Whilst local intrastriatal infusion of nicotine consistently elicits striatal dopamine release, systemic administration often fails to do so. Since chronic nicotine administration is known to result in desensitisation-induced upregulation of nicotinic acetylcholine receptors (nAChRs), the present study investigated whether chronic pre-treatment could enhance the response to systemic nicotine and, if so, whether increases in specific nAChR subunit mRNA levels in the substantia nigra pars compacta (SNc) may underlie this effect. In vivo microdialysis studies in male Sprague-Dawley rats revealed that following 4 days pre-treatment with nicotine (0.8 mg kg(-1)s.c.), local intrastriatal nicotine infusion (3 mM) elicited significantly higher dopamine efflux compared to vehicle pre-treated controls (peak release: 1273 +/- 199% basal versus 731 +/- 113% basal), whereas systemic nicotine challenge (0.8 mg kg(-1)s.c.) elicited no response. In contrast, following 8 days pre-treatment with nicotine (0.8 mg kg(-1)s.c.), systemic nicotine challenge (0.8 mg kg(-1)s.c.) now produced significantly higher dopamine efflux than that of vehicle pre-treated controls (147 +/- 30% basal versus 91 +/- 5% basal). Eight days pre-treatment with nicotine also significantly elevated the levels of alpha6 (approximately 55%) and beta3 (approximately 43%) nAChR subunit mRNA in the SNc, suggesting that up-regulation of these nAChR subunit genes in the nigrostriatal tract may contribute to the enhanced nicotine-evoked striatal dopamine release.

Animals↗

The adenosine A2A antagonist KF17837 reverses the locomotor suppression and tremulous jaw movements induced by haloperidol in rats: possible relevance to parkinsonism.

Recent evidence indicates that adenosine A2A receptors modulate the activity of striatal neurons, and that antagonists of this receptor may have actions in various animal models related to motor function. Four experiments were conducted to study the effects of systemic injections of the adenosine A2A antagonist KF17837 on the behavioral effects produced by repeated administration of the dopamine (DA) antagonist haloperidol. In the first two experiments, it was shown that repeated 0.5 mg/kg haloperidol severely suppressed open-field locomotor activity, and that KF17837 (0.0-20.0 mg/kg) did not significantly increase open-field locomotor activity. The third experiment demonstrated that injections of KF17837 (0.0-20.0 mg/kg) completely reversed the suppression of locomotion induced by haloperidol, and also increased rearing behavior in haloperidol-treated rats. Previous research has reported that haloperidol induces tremulous jaw movements that have many of the characteristics of parkinsonian tremor. The fourth experiment demonstrated that i.p. injections of KF17837 (0.0-20.0 mg/kg) also suppressed haloperidol-induced tremulous jaw movements. Taken together, the results of these experiments indicate that adenosine A2A antagonism can reverse the locomotor suppression and tremulous movements induced by DA antagonism. This profile of activity is consistent with the hypothesis that antagonism of adenosine A2A receptors can result in an antiparkinsonian effect in animal models.

Adenosine A2 Receptor Antagonists↗

Fluoxetine-induced change in rat brain expression of brain-derived neurotrophic factor varies depending on length of treatment.

Recent studies indicate that brain-derived neurotrophic factor (BDNF) may be implicated in the clinical action of antidepressant drugs. Repeated (2-3 weeks) administration of antidepressant drugs increases BDNF gene expression. The onset of this response as well as concomitant effects on the corresponding BDNF protein is however, unclear. The present study investigated the effects of acute and chronic administration of the selective serotonin reuptake inhibitor, fluoxetine (10mg/kg p.o.), upon regional rat brain levels of BDNF mRNA and protein expression. To improve the clinical significance of the study, fluoxetine was administered orally and mRNA and protein levels were determined ex vivo using the techniques of in situ hybridisation histochemistry and immunocytochemistry respectively. Direct measurement of BDNF protein was also carried out using enzyme-linked immunosorbent assay (ELISA). Four days of once daily oral administration of fluoxetine induced decreases in BDNF mRNA (hippocampus, medial habenular and paraventricular thalamic nuclei). Whilst 7 days of treatment showed a non-significant increase in BDNF mRNA, there were marked and region-specific increases following 14 days of treatment. BDNF protein levels remained unaltered until 21 days of fluoxetine treatment, when the numbers of BDNF immunoreactive cells were increased, reaching significance in the pyramidal cell layer of CA1 and CA3 regions of Ammon's horn (CA1 and CA3) but not in the other sub-regions of the hippocampus. Indicative of the highly regional change within the hippocampus, the ELISA method failed to demonstrate significant up-regulation at 21 days, measuring levels of BDNF protein in the whole hippocampus. In contrast to the detected time dependent and biphasic response of the BDNF gene, activity-regulated, cytoskeletal-associated protein (Arc) mRNA showed a gradual increase during the 14-day course of treatment. The results presented here show that BDNF is expressed differentially depending on length of fluoxetine administration, which could contribute in explaining the slow onset of antidepressant activity observed with selective serotonin reuptake inhibitors.

Animals↗

Differences in the BOLD fMRI response to direct and indirect cortical stimulation in the rat.

Functional MRI (fMRI) exploits a relationship between neuronal activity, metabolism, and cerebral blood flow to functionally map the brain. We have developed a model of direct cortical stimulation in the rat that can be combined with fMRI and used to compare the hemodynamic responses to direct and indirect cortical stimulation. Unilateral electrical stimulation of the rat hindpaw motor cortex, via stereotaxically positioned carbon-fiber electrodes, yielded blood oxygenation level-dependent (BOLD) fMRI signal changes in both the stimulated and homotypic contralateral motor cortices. The maximal signal intensity change in both cortices was similar (stimulated = 3.7 +/- 1.7%; contralateral = 3.2 +/- 1.0%), although the response duration in the directly stimulated cortex was significantly longer (48.1 +/- 5.7 sec vs. 19.0 +/- 5.3 sec). Activation of the contralateral cortex is likely to occur via stimulation of corticocortical pathways, as distinct from direct electrical stimulation, and the response profile is similar to that observed in remote (e.g., forepaw) stimulation fMRI studies. Differences in the neuronal pool activated, or neurovascular mediators released, may account for the more prolonged BOLD response observed in the directly stimulated cortex. This work demonstrates the combination of direct cortical stimulation in the rat with fMRI and thus extends the scope of rodent fMRI into brain regions inaccessible to peripheral stimulation techniques.

Animals↗

The role of neuronal nicotinic acetylcholine receptors in acute and chronic neurodegeneration.

In the last five years there has been a rapid explosion of publications reporting that neuronal nicotinic acetylcholine receptors (nAChRs) play a role in neurodegenerative disorders. Furthermore, there is a well-established loss of nAChRs in post-mortem brains from patients with Alzheimer's disease, Parkinson's disease and a range of other disorders. In the present review we discuss the evidence that nicotine and subtype selective nAChR ligands can provide neuroprotection in in vitro cell culture systems and in in vivo studies in animal models of such disorders. Whilst in vitro data pertaining to a protective effect of nicotine against nigral neurotoxins like MPTP is less robust, most studies agree that nicotine is protective against glutamate and beta-amyloid toxicity in various culture systems. This effect appears to be mediated by alpha7 subtype nAChRs since the protection is blocked by alpha-bungarotoxin and is mimicked by alpha7 selective agonists. In vivo studies indicate that alpha7 receptors play a critical role in protection from cholinergic lesions and enhancing cognitive function. The exact subtype involved in the neuroprotectant effects seen in animal models of Parkinson's disease is not clear, but in general broad spectrum nAChR agonists appear to provide protection, while alpha4beta2 receptors appear to mediate symptomatic improvements. Evidence favouring a protectant effect of nicotine against acute degenerative conditions is less strong, though some protection has been observed with nicotine pre-treatment in global ischaemia models. A variety of cellular mechanisms ranging from the production of growth factors through to inactivation of toxins and antioxidant actions of nicotine have been proposed to underlie the nAChR-mediated neuroprotection in vitro and in vivo. In summary, although the lack of subtype selective ligands has hampered progress, it is clear that in the future neuronal nAChR agonists could provide functional improvements and slow or halt the progress of several crippling degenerative diseases.

Acute Disease↗

Olanzapine activates the rat locus coeruleus: in vivo electrophysiology and c-Fos immunoreactivity.

BACKGROUND: Activation of central noradrenergic pathways by atypical antipsychotics has been hypothesized to play a role in their efficacy in treating the negative symptoms and cognitive impairment of schizophrenia. Because acute administration of the atypical antipsychotic olanzapine has been shown to increase extracellular levels of norepinephrine in the medial prefrontal cortex, we examined the effects of olanzapine on the noradrenergic cells of the locus coeruleus (LC). METHODS: The effects of olanzapine (0.25-16 mg kg(-1), IV) on the firing rates and patterns of LC neurons were determined by extracellular, single-unit recordings in chloral hydrate-anaesthetized rats. The effects of olanzapine and clozapine on c-Fos expression in the LC, nucleus subcoeruleus part alpha (SubCA), and nucleus A5 (A5) were studied by immunohistochemistry. RESULTS: Olanzapine increased LC cell firing rates, de-regularized firing, and induced burst firing. Induction of c-Fos expression in the LC by olanzapine and clozapine was confirmed and was also found in the SubCA, but not in A5. CONCLUSIONS: Acute administration of olanzapine activates the noradrenergic neurons of the rat LC. This increased activity of LC neurons may play an important role in the efficacy of olanzapine and clozapine in treating both the negative symptoms and cognitive impairment observed in schizophrenic patients.

Animals↗

LY393615, a novel neuronal Ca(2+) and Na(+) channel blocker with neuroprotective effects in models of in vitro and in vivo cerebral ischemia.

In the present studies we have examined the effects of a new calcium channel blocker, LY393615 ((N-Butyl-[5,5-bis-(4-fluorophenyl)tetrahydrofuran-2-yl]methylamine hydrochloride, NCC1048) in a model of hypoxia-hypoglycaemia in vitro and in a gerbil model of global and in two rat models of focal cerebral ischaemia in vivo. Results indicated that LY393615 protected against hypoxia-hypoglycaemic insults in brain slices and also provided significant protection against ischaemia-induced hippocampal damage in gerbil global cerebral ischaemia when dosed at 10, 12.5 (P<0.05) or 15 mg/kg i.p. (P<0.01) 30 min before and 2 h 30 min after occlusion. The compound penetrated the brain well after a 15 mg/kg i.p. dose and had a half-life of 2.5 h. In further studies LY393615 was protective 1 h post-occlusion when administered at 15 mg/kg i.p. followed by 2 doses of 5 mg/kg i.p. 2 and 3 h later. LY393615 dosed at 15 mg/kg i.p. followed by 2 further doses of 5 mg/kg i.p. (2 and 3 h later) also produced a significant reduction in the infarct volume following Endothelin-1 (Et-1) middle cerebral artery occlusion in the rat when administration was initiated immediately (P<0.01) or 1 h (P<0.05) after occlusion. The compound was also evaluated in the intraluminal monofilament model of focal ischaemia. The animals had the middle cerebral artery occluded for 2 h, and 15 min after reperfusion LY393615 was administered at 15 mg/kg i.p. followed by 2 mg/kg/h i.v. infusion for 6 h. There was no reduction in infarct volume using this dosing protocol. In conclusion, in the present studies we have reported that a novel calcium channel blocker, LY393615, with good bioavailability protects against neuronal damage caused by hypoxia-hypoglycaemia in vitro and both global and focal cerebral ischaemia in vivo. The compound is neuroprotective when administered post-occlusion and may therefore be a useful anti-ischaemic agent.

Animals↗

The effects of LY393613, nimodipine and verapamil, in focal cerebral ischaemia.

This study evaluates the effects of N-(2-[bis (4-fluorophenyl)methoxy]ethyl)-1-butanamine hydrochloride (LY393613), a novel neuronal (N/P/Q-type) Ca(2+) channel blocker, in ischaemia. For comparison, two commonly used L-type Ca(2+) channel blockers; nimodipine and verapamil were also evaluated. Ischaemia was induced in freely moving rats by micro-injection of endothelin-1 near the middle cerebral artery. In vivo microdialysis, laser Doppler flowmetry and histology were used to monitor ischaemia. Administration of LY393613, before and after the insult, attenuated the ischaemia-induced glutamate release, but not the dopamine release. Both nimodipine and verapamil failed to affect transmitter releases significantly, when administered post-occlusion. None of the compounds tested, produced any significant change in striatal blood flow. Histology showed that ischaemic damage was significantly less in LY393613 pre-treated rats. In conclusion, LY393613, a neuronal N/P/Q-Ca(2+) channel blocker, can attenuate ischaemic brain damage. The protective mechanism appears to be mainly the attenuation of the ischaemia-induced glutamate release, rather than its effect on cerebral hemodynamics.

Amines↗

Diffusion-weighted magnetic resonance imaging detects early neuropathology following four vessel occlusion ischemia in the rat.

Early neuropathology following a prolonged duration of four-vessel occlusion (4 VO) ischemia in the rat was charted using magnetic resonance imaging (MRI). Animals received either 30 minutes of 4 VO (N = 6) or sham operation (N = 6) prior to in vivo assessment. Proton density and T(2) and combined T(2)/diffusion-weighted (T(2)/DW) MRI were performed at 6, 24, and 72 hours postocclusion. T(2)/DW imaging was the most effective sequence for delineating between injured and intact tissues, indicating neuropathology in the dorsolateral striatum at 24 hours and in the CA1/CA2 subfields of the hippocampus at 72 hours following ischemia. Apparent diffusion coefficient values were significantly reduced in the striatum (P = 0.03) and hippocampus (P = 0.005) at 24 and 72 hours, respectively. This is the first report, to our knowledge, of T(2)/DW imaging detecting lesions following 4 VO in accord with the known temporal evolution of ischemic brain damage.

Animals↗

Modulation of the multidrug-resistance phenotype by new tropane alkaloid aromatic esters from Erythroxylum pervillei.

Nine tropane alkaloid aromatic esters (1-9) were isolated from the roots of Erythroxylum pervillei by following their potential to reverse multidrug-resistance with vinblastine-resistant oral epidermoid carcinoma (KB-V1) cells. All isolates, including seven new structures (3-9), were evaluated against a panel of human cancer cell lines, and it was found that alkaloids 3 and 5-9 showed the greatest activity with KB-V1 cells assessed in the presence of vinblastine, suggesting that these new compounds are potent modulators of P-glycoprotein. Confirmatory results were obtained with human ovarian adenocarcinoma (SKVLB) cells evaluated in the presence of adriamycin and synergistic studies performed with several cell lines from the NCI tumor panel. The structures of the new compounds were determined using spectroscopic techniques. Single-crystal X-ray analysis was performed on the monoester, tropane-3 alpha,6 beta,7 beta-triol 3-phenylacetate (1).

ATP Binding Cassette Transporter, Subfamily B↗

Nonvascular interventional procedures: analysis of a 10-year database containing more than 21,000 cases.

PURPOSE: To analyze all procedures performed during 10 years in a nonvascular interventional practice. MATERIALS AND METHODS: Date, organ location, and type of all 21,324 procedures performed between October 1990 and September 2000 were recorded in a database; also included were patient age and inpatient or outpatient status. Because genitourinary procedures were not included during the first 4 years, nephrostomies were added retrospectively. Yearly interventional caseload was compared with the department caseload and the assignment of new medical record numbers. Trends in individual procedure location and type were analyzed, as well as patient age, inpatient status, daily caseloads, and day of the week when the procedure was performed. RESULTS: Caseloads have increased 10.8% per year, exceeding increases in radiology department and hospital activity. Abdomen, outside of a specific organ, was the most common location; catheter deployment was the most common procedure. Abscess drainage, placement of chest tubes, and nephrostomies have increased, but biliary drainages have decreased. Inpatients outnumbered outpatients in all years except 1995, but the trend was toward an increase in the proportion of outpatients. The average patient was 59.6 years old, with average age diminishing. Friday was the busiest day, but weekend procedures have increased. CONCLUSION: Nonvascular interventional procedures have increased, with more currently being performed on weekends.

Databases, Factual↗

Tunneled peritoneal catheter placement under sonographic and fluoroscopic guidance in the palliative treatment of malignant ascites.

OBJECTIVE: We present a treatment for recurrent, symptomatic ascites in patients with malignant disease. This report summarizes our experience with percutaneous tunneled peritoneal catheters in 24 patients. SUBJECTS AND METHODS: Of the 40 consecutive patients who presented with at least four therapeutic paracenteses in a 4-week period, 24 patients underwent the percutaneous tunneled procedure. All had malignant ascites. RESULTS: All 24 patients had successful insertion of a permanent tunneled peritoneal drainage catheter. Eighteen were outpatients and six were inpatients. All patients were relieved of their clinical symptoms, including abdominal distention and dyspnea, and were relieved of lower extremity discomfort. The mean life span after catheter placement was 7.2 weeks. Twenty (83%) of the 24 patients were treated at home with their catheters in place. Three patients experienced minor complications from bacterial peritonitis, which responded to antibiotics. One patient had to have his catheter removed. CONCLUSION: Percutaneous placement of specialized tunneled catheters appears to be a viable and safe technique in patients who have symptomatic ascites that require frequent therapeutic paracentesis for relief of symptoms.

Adult↗

Neuroprotective effects of the neuronal Ca(2+) channel blockers, LY042826 and LY393615 in vivo.

In the present studies, we have examined the effects of two new Ca(2+) channel blockers, LY042826 (N-[2-[(2-methylphenyl)(phenyl)methoxy]ethyl]-1-butanamine hydrochloride) and LY393615 (N-[[5, 5-bis(4-fluorophenyl)tetrahydro-2-furanyl]methyl]-1-butanamine hydrochloride) in the gerbil model of global and the endothelin-1 rat model of focal cerebral ischaemia in vivo. Results indicated that both LY042826 (P<0.01) and LY393615 (P<0.001) provided significant protection against ischaemia-induced hippocampal damage in global cerebral ischaemia when dosed at 15 mg/kg i.p. 30 min before and 2 h 30 min after occlusion. In further studies, LY042826 (P<0.05) and LY393615 (P<0.01) were also protective when administered at 15 mg/kg i.p. immediately after and 3 h post-occlusion. Both compounds also provided a significant reduction in the infarct volume following endothelin-1 middle cerebral artery occlusion in the rat when administered at 15 mg/kg i.p. immediately (P<0.05) after occlusion. This protection was similar to that observed with the NMDA receptor antagonist (5R,10S)-(+)-5-methyl-10, 11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine), MK-801 in this model. In conclusion and as a result of the present studies, we report that the novel Ca(2+) channel blockers, LY042826 and LY393615 protect against ischaemia-induced brain injury in gerbils and rats. The compounds were neuroprotective when administered post-occlusion and may therefore be useful anti-ischaemic agents.

Animals↗

A model for predicting surgical outcome in patients with advanced ovarian carcinoma using computed tomography.

BACKGROUND: A reliable model for predicting the outcome of primary cytoreductive surgery may be a useful tool in the clinical management of patients with advanced epithelial ovarian carcinoma. METHODS: Forty-one women with a preoperative computed tomographic (CT) scan of the abdomen and pelvis and a histologic diagnosis of Stage III or IV epithelial ovarian carcinoma following primary surgery performed by one of nine gynecologic oncologists were identified from tumor registry databases. All CT scans were analyzed retrospectively using a panel of 25 radiographic features without knowledge of the operative findings. Patient demographics, surgical findings and outcome, Gynecologic Oncology Group performance status, and pre-operative serum CA125 values were collected from patient medical records. Residual disease measuring < or = 1 cm in maximal diameter was considered an optimal surgical result. Sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were calculated for each radiographic feature and clinical characteristic. Based on statistical probability of each factor predicting cytoreductive outcome, 13 radiographic features, in addition to performance status, were selected for inclusion in the final model. Each parameter was assigned a numeric value based on the strength of statistical association, and a total Predictive Index score was tabulated for each patient. Receiver operating characteristic (ROC) curve analysis was used to assess the ability of the model to predict surgical outcome. Statistical significance was evaluated using the Fisher exact test. RESULTS: Twenty of 41 patients (48.8%) underwent optimal cytoreduction to </= 1 cm residual disease. CT features of peritoneal thickening, peritoneal implants (>/= 2 cm), bowel mesentery involvement (>/= 2 cm), suprarenal paraaortic lymph nodes (>/= 1 cm), omental extension (spleen, stomach, or lesser sac), and pelvic sidewall involvement and/or hydroureter were most strongly associated with surgical outcome. Using the Predictive Index scores, a receiver operating characteristic curve was generated with an area under the curve = 0. 969 +/- 0.023. In the final model, a Predictive Index score >/= 4 had the highest overall accuracy at 92.7% and identified patients undergoing suboptimal surgery with a sensitivity of 100% (21/21). The specificity, or ability to identify patients undergoing optimal surgery, was 85.0% (17/20). The PPV of a Predictive Index score >/= 4 was 87.5% (21/24), and the NPV was 100%. The ability of this model to correctly predict surgical outcome was statistically significant (P < 0.001). CONCLUSIONS: In this model, a Predictive Index score >/= 4 demonstrated high sensitivity, specificity, PPV, and NPV, and was highly accurate in identifying patients with advanced epithelial ovarian carcinoma unlikely to undergo optimal primary cytoreductive surgery. The Predictive Index model may have clinical utility in guiding the management of patients with ovarian carcinoma.

Adult↗