Highly Atherogenic Lipid Particles are Associated with Preeclampsia After Successful Fertility Treatment for Obese Women who have Unexplained Infertility.

Atherogenic dyslipidemia-before or during pregnancy-may contribute to preeclampsia and subsequent cardiovascular disease risk. We performed a nested case-control study to further understand dyslipidemia associated with preeclampsia. The cohort consisted of participants in the randomized clinical trial "Improving Reproductive Fitness Through Pretreatment with Lifestyle Modification in Obese Women with Unexplained Infertility" (FIT-PLESE). FIT-PLESE was designed to study the effect of a pre-fertility treatment 16-week randomized lifestyle intervention program (Nutrisystem diet + exercise + orlistat vs. training alone) on improvement in live birth rate among obese women with unexplained infertility. Of the 279 patients in FIT-PLESE, 80 delivered a viable infant. Maternal serum was analyzed across five visits: before and after lifestyle interventions and also at three pregnancy visits (16, 24, and 32 weeks gestation). Apolipoprotein lipids were measured in a blinded fashion using ion mobility. Cases were those who developed preeclampsia. Controls also had a live birth but did not develop preeclampsia. Generalized linear and mixed models with repeated measures were used to compare the mean lipoprotein lipid levels of the two groups across all visits. Complete data were available for 75 pregnancies, and preeclampsia developed in 14.5% of the pregnancies. Cholesterol/high-density lipoprotein (HDL) ratios (p < 0.003), triglycerides (p = 0.012), and triglyceride/HDL ratios, all adjusted for BMI, were worse in patients with preeclampsia (p < 0.001). Subclasses a, b, and c of highly atherogenic, very small, low-density lipoprotein (LDL) particles were higher during pregnancy for the preeclamptic women (p < 0.05). Very small LDL particle subclass d levels were significantly greater only at 24 weeks (p = 0.012). The role of highly atherogenic, very small LDL particle excess in the pathophysiology of preeclampsia awaits further investigation.

Proprotein Convertase Subtilisin Kexin 9 (PCSK9) and nonHDL particles rise during normal pregnancy and differ by BMI.

BACKGROUND: Serum lipids, including total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-c), increase during pregnancy. Serum Proprotein Convertase Subtilisin Kexin 9 (PCSK9) is a vital regulator in lipoprotein metabolism. Circulating PCSK9 downregulates the LDL receptor on the surface of liver cells inhibiting clearance of LDL-c. OBJECTIVE: To determine the influence of weeks of pregnancy and obesity on circulating levels of essential lipid lipoproteins and PCSK9 in women with normal, uncomplicated pregnancies and deliveries. METHODS: We performed a comprehensive lipid and lipoprotein profile during each trimester of pregnancy in 70 mostly Caucasian women with uncomplicated normal pregnancies and deliveries. Based on their first trimester BMI, we placed them into one of three categories: (<25 kg/m2 n=23, 25-30 kg/m2 n=25, or >30 n=22) kg/m2. Cholesterol, triglycerides, LDL cholesterol (LDL-c), non-HDL particles, and lipoprotein(a) were measured by spectrophotometry, ion mobility, and immunoturbidimetric assays. Elisa assay determined PCSK9 (active and total). Homeostatic Model Assessment (HOMA-IR) assessed insulin resistance in the second and third trimesters of pregnancy. RESULTS: Total and active PCSK9, LDL-c, and nonHDL particle concentrations were higher than reported for non-pregnant normal values, increased after the first trimester of pregnancy, and were highest from mid-gestation to the last trimester of pregnancy in the overweight and the obese. CONCLUSION: PCSK9 levels rise as normal pregnancy progresses. Levels are higher in persons who are obese, even after adjustment for insulin resistance. Defining normal PCSK9 levels during pregnancy must adjust for gestational age and BMI.

Prevalence of lameness in sheep transported to meat processing plants in New Zealand and associated risk factors.

Aims: To estimate the prevalence of lameness in sheep transported to meat processing plants in New Zealand, and to identify factors associated with the prevalence of lameness. Methods: The survey was conducted over the main meat processing season, running from October 2012 to the end of May 2013, at 10 sheep processing premises (five North Island and five South Island). A sample of 50 sheep selected from approximately six sheep consignments per week from each of the processing plants were scored for lameness, using a scale from Grade 1 (mild) to 3 (severe, non-weight-bearing). For each consignment the breed, age class and mean carcass weight were recorded. A multivariable regression model was fitted to identify the risk factors for prevalence of lame sheep (Grade 1-3) within a consignment. Results: In total, 1,854/78,833 (2.4 (95% CI = 2.2-2.5)%) sheep were diagnosed with lameness. Of the 1,854 lame sheep, lameness severity was Grade 1 in 1,349 (72.8%), Grade 2 in 450 (24.3%) and Grade 3 in 55 (3.0%) sheep. Within consignments ≥1 lame sheep was observed in 600/1,682 (35.7 (95% CI = 33.4-38.0)%) consignments. In Merino lambs and ewes the prevalence of lameness was greater than that of other breeds (p < 0.001), but in rams/wethers, the prevalence of lameness was lower in Merino than other breeds (p < 0.05). In sheep originating from the North Island, increasing mean carcass weight was associated with an increase in the prevalence of lameness (p < 0.001), but in the South Island prevalence was similar for different carcass weights (p = 0.5). In the North Island increasing yarding time was associated with an increase in the lameness prevalence (p < 0.01), but not in the South Island (p = 0.7). Sheep from the South Island generally had a higher prevalence of lameness than the North Island and the prevalence of lameness was lower over summer and autumn relative to the previous spring (p < 0.01). Conclusion: The results from this survey provided a measure of the prevalence of lameness in a section of the New Zealand sheep population, namely those animals sent for slaughter; as well as identification of several risk factors associated with lameness.

Contribution of human-related sources to indoor volatile organic compounds in a university classroom.

Although significant progress has been made in understanding the sources and chemistry of indoor volatile organic compounds (VOCs) during the past decades, much is unknown about the role of humans in indoor air chemistry. In the spring of 2014, we conducted continuous measurements of VOCs using a proton transfer reaction mass spectrometer (PTR-MS) in a university classroom. Positive matrix factorization (PMF) of the measured VOCs revealed a 'human influence' component, which likely represented VOCs produced from human breath and ozonolysis of human skin lipids. The concentration of the human influence component increased with the number of occupants and decreased with ventilation rate in a similar way to CO2 , with an average contribution of 40% to the measured daytime VOC concentration. In addition, the human skin lipid ozonolysis products were observed to correlate with CO2 and anticorrelate with O3 , suggesting that reactions on human surfaces may be important sources of indoor VOCs and sinks for indoor O3 . Our study suggests that humans can substantially affect VOC composition and oxidative capacity in indoor environments.

Measurements of Tan's contact in an atomic Bose-Einstein condensate.

A powerful set of universal relations, centered on a quantity called the contact, connects the strength of short-range two-body correlations to the thermodynamics of a many-body system with zero-range interactions. We report on measurements of the contact, using rf spectroscopy, for an (85)Rb atomic Bose-Einstein condensate (BEC). For bosons, the fact that contact spectroscopy can be used to probe the gas on short time scales is useful given the decreasing stability of BECs with increasing interactions. A complication is the added possibility, for bosons, of three-body interactions. In investigating this issue, we have located an Efimov resonance for (85)Rb atoms with loss measurements and thus determined the three-body interaction parameter. In our contact spectroscopy, in a region of observable beyond-mean-field effects, we find no measurable contribution from three-body physics.

Bragg spectroscopy of a strongly interacting 85Rb Bose-Einstein condensate.

We report on measurements of the excitation spectrum of a strongly interacting Bose-Einstein condensate. A magnetic-field Feshbach resonance is used to tune atom-atom interactions in the condensate and to reach a regime where quantum depletion and beyond mean-field corrections to the condensate chemical potential are significant. We use two-photon Bragg spectroscopy to probe the condensate excitation spectrum; our results demonstrate the onset of beyond mean-field effects in a gaseous Bose-Einstein condensate.

Measurement of the temperature dependence of the Casimir-Polder force.

We report on the first measurement of a temperature dependence of the Casimir-Polder force. This measurement was obtained by positioning a nearly pure 87Rb Bose-Einstein condensate a few microns from a dielectric substrate and exciting its dipole oscillation. Changes in the collective oscillation frequency of the magnetically trapped atoms result from spatial variations in the surface-atom force. In our experiment, the dielectric substrate is heated up to 605 K, while the surrounding environment is kept near room temperature (310 K). The effect of the Casimir-Polder force is measured to be nearly 3 times larger for a 605 K substrate than for a room-temperature substrate, showing a clear temperature dependence in agreement with theory.

Correlation of pharmacokinetics with the antitumor activity of Cetuximab in nude mice bearing the GEO human colon carcinoma xenograft.

PURPOSE: The epidermal growth factor receptor (EGFR), a protein tyrosine kinase expressed in many types of human cancers including colon and breast, has been strongly associated with tumor progression. Cetuximab, an IgG1 anti-EGFR chimeric mouse/human monoclonal antibody, has been proven to be effective in the treatment of advanced colon cancer. To date, there has not been a study to systematically evaluate the pharmacokinetics (PK) of Cetuximab in a preclinical model and to further explore any correlation of drug exposure between animal models and cancer patients. In the present study, we characterized the PK of Cetuximab in nude mice at efficacious dose levels and further compared the preclinical optimal dose and active plasma drug concentration with those determined in clinical studies. EXPERIMENTAL DESIGN: The antitumor activity of Cetuximab was evaluated using the GEO human colon carcinoma xenografts implanted subcutaneously in nude mice. The drug was administered ip every 3 days for five total injections (inj) (q3dx5) at dose levels ranging from 1 mg/inj to 0.04 mg/inj. The plasma PK of Cetuximab was determined at dose levels of 1.0, 0.25, and 0.04 mg/inj with a single bolus iv or ip administration in nude mice. The tumoral PK of Cetuximab was determined at dose levels of 0.25, and 0.04 mg/inj with a single bolus ip administration in nude mice bearing GEO tumor xenografts. The plasma and tumoral levels of Cetuximab were quantitated by an ELISA assay. RESULTS: Cetuximab demonstrated a dose-dependent antitumor activity at dose levels of 0.25, 0.1, and 0.04 mg/inj, with a statistically significant tumor growth delay (in reaching a tumor target size of 1 gm) of 18 days (P < 0.001), 12.3 days (P < 0.01), and 10 days (P < 0.01) for 0.25, 0.1, and 0.04 mg/inj, respectively. A separate study employing the same treatment schedule showed that Cetuximab was equally active at dose levels ranging from 0.25 mg/inj to 1 mg/inj. Therefore, dose levels of Cetuximab from 1 mg/inj to 0.04 mg/inj can be considered to be within the efficacious range, while dose levels of 0.25 mg/inj or higher appeared to be optimal for the antitumor activity of Cetuximab in the GEO tumor model. When Cetuximab was given iv to mice, the elimination half life (t(1/2)) was 39.6, 37.8, and 42.2 h for doses of 1.0, 0.25, and 0.04 mg/inj, respectively, suggesting a similar disposition kinetics of Cetuximab within this dose range. The volume of distribution (V(d)) ranged from 0.062 l/kg to 0.070 l/kg, suggesting that Cetuximab is primarily confined to the plasma compartment with limited peripheral tissue distribution. Clearance (CL) was similar and no apparent PK saturation was observed across the dose ranging from 0.04 mg/inj to 1.0 mg/inj. When mice were administered with a single bolus ip administration at doses of 1, 0.25, and 0.04 mg/inj, the maximum plasma concentration (C(max)) was 407.6, 66.4, and 16.5 microg/ml. The area under the curve of plasma drug concentration (AUC) was 19212.4, 3182.4, and 534.5 microg/ml h, for 1.0, 0.25, and 0.04 mg/inj, respectively. The average steady state plasma concentration (C(ss avg)) for the multiple dosing schedule was estimated to be 73.1 microg/ml at 0.25 mg/inj and was considered as an active plasma drug concentration. The maximum tumoral concentration of Cetuximab was 2.6 and 0.53 ng/mg-tumor while the tumoral drug exposure was 112.6 and 18.3 ng/mg h for 0.25 and 0.04 mg/inj, respectively. The EGFR was estimated to be nearly completely occupied by Cetuximab at the optimal dose of 0.25 mg/inj. CONCLUSION: In the present study, we compared the preclinical optimal dose and the corresponding active plasma concentration determined in mice with those being observed in cancer patients, i.e. 65-100 microg/ml. The preclinical optimal dose of 0.25 mg/inj was significantly lower than the current clinical dose. However, the active plasma concentration at 0.25 mg/inj is within the range of the active drug concentrations in cancer patients treated with Cetuximab under the current optimal dosing regimen. It appears that the active plasma drug concentration determined in preclinical model predicts better than the optimal preclinical dose for the clinical development of antibody drugs.

VEGF-DT385 toxin conjugate inhibits mammary adenocarcinoma development in a transgenic mouse model of spontaneous tumorigenesis.

Previous experiments have shown that a vascular endothelial growth factor (VEGF)-DT385 toxin conjugate inhibits endothelial cell proliferation, angiogenesis and solid tumor growth in a xenotransplant model system. Here, we report that VEGF-DT385 toxin conjugate effectively inhibits spontaneous tumorigenesis. The C3(1)/SV40 TAg transgenic mouse model of mammary gland carcinogenesis was used to determine the effectiveness of VEGF-DT385 toxin conjugate in delaying the onset of disease and the development of solid tumors. Animals were treated daily with conjugate for a period of 7 days. Therapy was initiated at week 14 of development before any visible adenocarcinomas were evident. Treatment of mice with VEGF-DT385 toxin conjugate significantly delayed the onset of tumorigenesis and inhibited solid tumor growth by more than 92%. Furthermore, conjugate treated animals showed less than twice the number of tumor nodules when compared to control mice. Finally, this vascular targeting agent significantly increased survival time of animals by 5 weeks. VEGF-DT385 toxin conjugate resulted in temporary weight loss and no long-lasting toxicity was seen. More importantly, using this established tumor model, VEGF-DT385 toxin conjugate appeared to be as effective as a similar treatment schedule with recombinant human endostatin. Our results suggest that VEGF-DT385 toxin conjugate is a potent inhibitor of mammary adenocarcinoma growth and might be useful in breast cancer therapy.

Cholinesterase inhibitors for dementia with Lewy bodies.

BACKGROUND: Dementia with Lewy bodies (DLB) was first described in 1983, and clinical diagnostic criteria were published in the early to mid 1990s. It has been suggested DLB may account for up to 15-25% of cases of dementia among people aged over 65, although autopsy suggests much lower rates. Characteristic symptoms are dementia, marked fluctuation of cognitive ability, early and persistent visual hallucinations and spontaneous motor features of Parkinsonism. Falls, syncope, transient disturbances of consciousness, neuroleptic sensitivity, and hallucinations in other modalities are also common. This combination of features can be difficult to manage as neuroleptics can make the Parkinsonian and cognitive symptoms worse. There is evidence to suggest that the cholinesterase inhibitors may be beneficial in this disorder; small case series indicate that cholinesterase inhibitors are safe, and will improve both cognitive deficits and neuropsychiatric symptoms in DLB. OBJECTIVES: To assess the use of cholinesterase inhibitors in DLB. SEARCH STRATEGY: The trials were identified from a search of the Specialized Register of the Cochrane Dementia and Cognitive Improvement Group on 25 February 2002 using the terms 'lewy body', 'Lewy bodies' and 'Lewy'. This register contains records from all major health care databases and trial databases and is updated regularly. SELECTION CRITERIA: Randomized, double-blind trials in which treatment with cholinesterase inhibitors was administered and compared with alternative interventions in patients with DLB are included. DATA COLLECTION AND ANALYSIS: Two reviewers (TP, RW) independently assessed quality of trials according to criteria described in the Cochrane Collaboration Handbook. Each drug was to be examined separately, and together as a group. We also analysed data by time to outcome measurement; short-term (up to one month), medium term (one month up to six months) and long term (Six months and longer). The primary outcome measures of interest are in the following areas: neuropsychiatric features. i.e. psychiatric symptoms and behavioural disturbances, cognitive function, activities of daily living, global assessments, quality of life, including maintaining role and social functioning, effect on carers, safety as measured by incidence of adverse events and side effects, acceptability of treatment as measured by withdrawal from trials, and by patient/carer assessment, institutionalization and death. MAIN RESULTS: There was one included trial (McKeith 2000f) of rivastigmine compared with placebo on 120 patients. Neuropsychiatric InventoryThe 10-item test found no significant difference between the two groups in change of scores from baseline using intention-to-treat (ITT) analysis at 20 weeks and last observation carried forward (LOCF) analysis. The treatment effect was statistically significant in favour of rivastigmine if only observed cases (OC) were analysed (WMD -6.94, 95% CI -11.59 to -2.29, P=0.003). There were similar results for the NPI-4, with only the OC analysis showing a significant superiority of rivastigmine to placebo at 20 weeks (WMD -3.75, 95%CI -6.62 to -0.88, P=0.01).MMSE:Analysis of these results showed no statistically significant difference between the two groups at 20 weeks.CGC-plus:Analysis of the proportion of patients who had no change or became worse found no statistically significant difference between the two groups at 20 weeks for the ITT, LOCK and OC analyses. Adverse Events:The placebo group experienced significantly fewer adverse events than the treatment group (54/59 vs 46/61,OR 3.52, 95%CI 1.19 to 10.43). However, using ITT analysis of 20-week data, there was no significant difference between the two groups when serious adverse events were considered. There were no significant differences in death rates between the two groups at 20 weeks.Drop-out Rates:Analysis of these results showed no difference between the two groups at 20 weeks using ITT analysis. REVIEWER'S CONCLUSIONS: Patients with dementia with Lewy bodies who suffer from behavioural disturbance oS CONCLUSIONS: Patients with dementia with Lewy bodies who suffer from behavioural disturbance or psychiatric problems may benefit from rivastigmine if they tolerate it, but the evidence is weak. Further trials using rivastigmine are needed, as are trials of other cholinesterase inhibitors in dementia with Lewy bodies.

Estrogens, progestins, selective estrogen receptor modulators, and the arterial tree.

We reviewed studies of the effects of different estrogens, progestins, and selective estrogen receptor modulators at the coronary and carotid arterial sites to help determine their likely effects on cardiovascular morbidity and mortality. All English-language studies published between 1997 and 2000 on MEDLINE, Current Contents, and Best Evidence were reviewed, including in vitro, other animal, human physiologic, and clinical trial studies. We synthesize, assess limitations, and integrate across systems with the in vivo experience in humans to evaluate the clinical context. Estrogens have favorable direct effects in most circumstances, progestins oppose these effects, and early studies suggest that selective estrogen receptor modulators are protective. In some systems the dosage, route of delivery, and type of progestin may be important and risk factors may modulate hormone effects. The evaluation of endothelial dysfunction gives a unique in vivo opportunity to assess the vascular properties of hormones, although the relationship between the in vivo physiologic effects of hormones and clinical outcomes remains to be determined.

Inhibition of angiogenesis and tumour growth by VEGF121-toxin conjugate: differential effect on proliferating endothelial cells.

Vascular endothelial growth factor (VEGF) plays an important role in tumour angiogenesis. VEGF binds to tyrosine kinase receptors, which are expressed almost exclusively on tumour endothelium. Therefore, VEGF can be used to target toxin molecules to tumour vessels for anti-angiogenic therapy. However, recent evidence suggests that VEGF can also bind in an isoform-specific fashion to a newly identified neuropilin-1 (NP-1) receptor. NP-1 is widely expressed in normal tissue and presents a potential target for unwanted toxicity. As a consequence, we investigated whether the VEGF121 isoform, which lacks the NP-1 binding domain, could be used to target toxin polypeptides to tumour vasculature. Treatment of endothelial cells with a VEGF121-diphtheria toxin (DT385) conjugate selectively inhibited proliferating endothelial cells, whereas confluent cultures were completely resistant to the construct. In addition, VEGF121-DT385 conjugate treatment completely prevented tumour cell induced angiogenesis in vivo. Most importantly, the conjugate inhibited tumour growth in athymic mice and induced tumour-specific vascular damage. There was also no apparent toxicity associated with the treatment. Our results suggest that proliferating endothelial cells are highly sensitive to VEGF121-toxin conjugates and that the binding to NP-1 receptors is not necessary for efficient inhibition of tumour growth.

Quantitative assessment of angiogenesis and tumor vessel architecture by computer-assisted digital image analysis: effects of VEGF-toxin conjugate on tumor microvessel density.

Tumor growth is angiogenesis dependent. As a consequence, strategies aimed at disrupting this mechanism are heavily investigated. Several angiogenesis assays are used to directly compare the efficacy of anti-angiogenic compounds. However, objective assessment of new vascular growth has been difficult to achieve. The aim of this study was to test and develop a computer-assisted image analysis method that would give an unbiased quantification of the microvessel density. Human tumors were grown in athymic mice and tumor biopsies were taken after a weeklong treatment with VEGF-toxin conjugate. Frozen tumor sections were prepared and stained with PE-conjugated anti-CD-31 antibodies and vessels were imaged with a fluorescence microscope. Vessel density was analyzed by quantifying PE-positive pixels per recorded field. In addition, images were further processed to investigate morphological differences by an automated binarization and skeletonization protocol. This procedure allowed the computer-assisted estimation of important angiogenic parameters such as total vessel number, length, and branch points. Based on these indices, differences in the angiogenic response between control tumors and those treated with VEGF-toxin conjugate were readily detected (P < 0.007 for all parameters). More importantly, computer-generated measurements correlated well with manual microvessel counts and showed significantly less variation. Our results suggest that computer-assisted image analysis represents a rapid, objective, and alternative method for the quantitative assessment of tumor angiogenesis and vessel architecture.

The effects of hormone replacement therapy and raloxifene on C-reactive protein and homocysteine in healthy postmenopausal women: a randomized, controlled trial.

C-Reactive protein and homocysteine are independent risk factors for the development of cardiovascular disease. This study compared the effects of hormone replacement therapy (HRT) and raloxifene on serum C-reactive protein and homocysteine levels as markers of cardiovascular risk in healthy postmenopausal women. Healthy postmenopausal women (n = 390) were enrolled in a double blind, randomized, placebo-controlled, 6-month trial at eight out-patient sites in the United States. Women were randomly assigned to receive continuous combined HRT (0.625 mg/day conjugated equine estrogen and 2.5 mg/day medroxyprogesterone acetate), raloxifene (60 or 120 mg/day), or placebo for 6 months. C-Reactive protein and homocysteine were measured in baseline and 6-month serum samples. HRT increased C-reactive protein levels by 84% (P<0.001), whereas raloxifene (60 and 120 mg/day) had no significant effect (-6% and -4%;, respectively; P>0.2). Raloxifene (60 and 120 mg/day) significantly lowered serum levels ofhomocysteine by 8% (P = 0.014) and 6% (P = 0.024), respectively, similar to the 7% (P = 0.014) reduction obtained with HRT. We conclude that HRT and raloxifene lower serum homocysteine levels to a comparable extent in postmenopausal women. Whereas cardiovascular risk predicted by C-reactive protein in healthy postmenopausal women is not influenced by raloxifene, the relationship between elevated C-reactive protein levels with HRT and cardiovascular disease events requires further study.

Krill protease effects on wound healing after corneal alkali burn.

PURPOSE: To study the effect of a novel protease in the development and progression of corneal ulceration secondary to alkali burning. METHODS: By using a 4N alkali burn model of corneal ulceration in rabbits, the effects and efficacy of topical application of a novel protease (PHM-101) capable of degrading metalloproteinases was studied for 28 days of treatment and 7 days off treatment for its effect on corneal ulceration and recurrent erosion. RESULTS: At day 28, both the protease- and placebo-treated groups had different numbers of eyes showing reepithelialization (nine (45%) of 20 and six (33%) of 18, respectively]. By day 35 the protease-treated group had significantly fewer recurrent epithelial defects [two (13%) of 15 vs. eight (61%) of 13; p = 0.02]. Similarly, at day 35 the protease-treated group showed significantly less corneal ulceration [two (13%) of 15 vs. six (46%) of 13; p = 0.02], and those ulcers were of a lesser severity (three units vs. 17.76 units). No difference was found in the degree of stromal edema or neovascularization, nor was there any difference in histopathologic characteristics of inflammatory cell infiltration and corneal scarring. CONCLUSION: We conclude that this novel protease is efficient in reducing recurrent corneal epithelial defects and stromal ulceration after alkali burning.

[Frozen-section biopsy in ovarian neoplasm diagnosis: diagnostic correlation according to diameter and weight in tumors of epithelial origin]. / Biopsia rápida por congelación en el diagnóstico de tumores de ovario: correlación diagnóstica según diámetro y peso en tumores de origen epitelial.

BACKGROUND: Adequate management and treatment of ovarian carcinoma requires a complete surgical staging supported by frozen-section examination. To achieve this goal it is necessary a high level of accuracy. AIM: To evaluate the accuracy of frozen-sections in ovarian carcinoma considering the influence of tumor diameter and weight. PATIENTS AND METHODS: Retrospective study of frozen-sections performed in patients with ovarian tumors who underwent surgery. Frozen- and permanent-sections were divided into three categories (benign, borderline and malignant) and stratified by diameter (< 10 cm, 10 to 20 cm, > 20 cm) and weight (< 700 g, 700 a 1400 g, > 1400 g). The diagnostic correlation, sensitivity, specificity, predictive values and accuracy of each frozen-section diagnosis were determined. RESULTS: Eight hundred forty two ovarian tumors that underwent frozen-sections between January 1988 and October 1998 were studied. Final diagnosis was 86.7% benign, 2.7% low malignant potential (LMP) and 10.6% malignant. The diagnosis correlation between frozen- and permanent-sections was 98.2%. Misdiagnosis was in epithelial ovarian tumors, particularly in LMP tumors. Sensitivity, specificity, positive- and negative-predictive values and accuracy of the four hundred eighty nine epithelial tumor were 92.6%, 99.2%, 96.7%, 98.2% and 97.9%, respectively. Diagnostic correlation was higher in epithelial ovarian tumors with diameter < 10 cm (98.2% v/s 93.8%) and weight < 700 g (96.9% v/s 88.9%). CONCLUSIONS: Diagnostic correlation with permanent-section examination, sensitivity, specificity and predictive values of frozen-sections are high in ovarian tumors. Accurate diagnosis at frozen sections of epithelial ovarian tumors with diameter > 10 cm or weight > 700 g (particularly in LMP tumors) is difficult because of the extensive sampling required. Frozen-sections diagnoses are important to determine the type and extent of surgery performed at the initial operation.