Survival analysis: A consumer-friendly method to estimate the optimum sucrose level in probiotic petit suisse.

For years, just-about-right (JAR) scales have been among the most used techniques to obtain sensory information about consumer perception, but recently, some researchers have harshly criticized the technique. The present study aimed to apply survival analysis to estimate the optimum sucrose concentration in probiotic petit suisse cheese and compare the survival analysis to JAR scales to verify which technique more accurately predicted the optimum sucrose concentration according to consumer acceptability. Two panels of consumers (total=170) performed affective tests to determine the optimal concentration of sucrose in probiotic petit suisse using 2 different methods of analysis: JAR scales (n=85) and survival analysis (n=85). Then an acceptance test was conducted using naïve consumers (n=100) between 18 and 60 yr old, with 2 samples of petit suisse, one with the ideal sucrose determined by JAR scales and the other with the ideal sucrose content determined by survival analysis, to determine which formulation was in accordance with consumer acceptability. The results indicate that the 2 sensory methods were equally effective in predicting the optimum sucrose level in probiotic petit suisse cheese, and no significant differences were detected in any of the characteristics related to liking evaluated. However, survival analysis has important advantages over the JAR scales. Survival analysis has shown the potential to be an advantageous tool for dairy companies because it was able to accurately predict the optimum sucrose content in a consumer-friendly way and was also practical for researchers because experimental sensory work is simpler and has been shown to be more cost effective than JAR scales without losses of consumer acceptability.

Influence of various traditional seasonings on beef flavor: United States, Spanish, and Argentinian practices.

A consumer study was conducted to determine the most popular beef seasonings used in three countries: Argentina, United States (US), and Spain. Once the typical cooking methods and seasonings in these countries were established, descriptive analysis was used to determine the differences in the main flavor attributes, particularly the impact on beef characteristics, of the samples. Large variations were found in the consumer practices in the studied countries, and the preferred seasonings from each country were identified. This study showed that on average US consumers would prefer beef products with more initial flavor impact, brown/roasted and salty characteristics than Argentinian or Spanish consumers. The addition of seasonings changed some of the main beef attributes, but the changes were dependent on the cooking method. Beef identity (Beef ID), brown/roasted, and bloody/serumy were the attributes most affected when adding different seasonings.

Optimum level of salt in French-type bread. Influence of income status, salt level in daily bread consumption, and test location.

The objectives of the present study were to measure the ideal salt concentration in French-type bread among Argentine consumers in a home-usage-test (HUT) considering income status and salt content of daily bread consumption as covariables, and to compare the ideal salt concentrations measured in a HUT and a central-location test (CLT). For the HUT, 420 consumers each received a sample of bread with a single salt concentration, and for the CLT, 100 consumers each received 7 samples with different salt concentrations. For each sample, consumers responded if they found the bread "not-salty-enough,""okay," or "too-salty." Neither income level nor salt content of daily bread influenced probability of rejection. The optimum sodium concentrations (milligrams per 100 g of bread dry basis) +/- 95% confidence limits for the HUT and CLT were 980 +/- 74 and 1157 +/- 87, respectively. These values are substantially higher than 628, the mean sodium content of the bread sampled from the bakery shops where consumers bought their daily bread.

Holstein-Friesian dairy cows under a predominantly grazing system: interaction between genotype and environment.

A 5 yr whole-system study, beginning in June 1994, compared the productivity of high [HGM; Australian Breeding Value (ABV) of 49.1 kg of fat plus protein] and low [LGM; ABV of 2.3 kg of fat plus protein] genetic merit cows. Cows from both groups were fed at 3 levels of concentrate (C): 0.34 (low C), 0.84 (medium C), and 1.71 (high C) t of DM/cow per lactation. Thus, there were 6 treatments (farmlets) composed of 18 cows each. The 30 blocks of pasture on each farmlet were matched between farmlets for pasture growth before the study (and soil characteristics and aspect). Cows were culled, and pasture and feed use were managed so as not to bias any one treatment. Genetic merit, level of feeding, and their interaction were significant effects for protein content, protein/cow, and milk and protein/ha. For fat and milk yield/cow, genetic merit and level of feeding were significant, whereas there was no significant effect of genetic merit on fat content. The difference of 46.8 kg of fat plus protein yield between the ABV of HGM and LGM cows and the actual difference in production between the 2 groups was not significantly different except for low C (27 kg) cows. This was due to a 3-fold lower protein yield difference (6 kg/cow) compared with an ABV difference for protein yield of 17.9 kg/cow. The dramatic effect of treatment on protein is in line with differences in the mean protein content (2.89% for the HGM - low C cows compared with a mean of 3.02% for the remaining groups) and mean body condition score [4.3 for HGM - low C cows compared with 4.8 for the mean of the remaining groups (scale 1 to 8)], both indicators reflecting a higher negative energy balance in the HGM - low C cows. When individual cow production was plotted against ABV for production of milk or protein yield all relationships were quadratic, but the slope was relatively flat (low response to ABV) for the low C cows, steeper for the medium C cows and steepest (but not linear) for the high C cows. The relationship between ABV for fat yield and actual fat yield was linear for all levels of concentrate. The mean milk yield/ha from pasture for the 6 farmlets over the 5 yr was 11,868 L, 11,417 L, or 7,761 L for the HGM cows fed at low C, medium C, or high C, respectively, and 10,579 L, 9,800 L, or 5,812 L for LGM cows, fed at low C, medium C, or high C, respectively. The response to concentrates fed was very high for the HGM - medium C cows at 0.115 kg fat plus protein or 1.75 L milk/kg of concentrate fed, with comparable figures of 0.083 kg and 1.0 L, 0.86 kg and 1.47 L and 0.066 and 0.92 L/kg of concentrate fed for the HGM - high C, LGM - medium C, and LGM - high C, respectively. The results show a significant genetic merit by environment (level of feeding) interaction for reproduction and most production parameters when considered in terms of the individual cow and the whole farm system.

Sensory shelf life of dulce de leche.

The objectives of this research were to determine the sensory cutoff points for dulce de leche (DL) critical descriptors, both for defective off-flavors and for storage changes in desirable attributes, and to estimate the shelf life of DL as a function of storage temperature. The critical descriptors used to determine the cutoff points were plastic flavor, burnt flavor, dark color, and spreadability. Linear correlations between sensory acceptability and trained panel scores were used to determine the sensory failure cutoff point for each descriptor. To estimate shelf life, DL samples were stored at 25, 37, and 45 degrees C. Plastic flavor was the first descriptor to reach its cutoff point at 25 degrees C and was used for shelf-life calculations. Plastic flavor vs. storage time followed zero-order reaction rate. Shelf-life estimations at different temperatures were 109 d at 25 degrees C, 53 d at 37 degrees C, and 9 d at 45 degrees C. The activation energy, necessary to calculate shelf lives at different temperatures, was 14,370 +/- 2080 cal/mol.

Consumer acceptability versus trained sensory panel scores of powdered milk shelf-life defects.

The objective of the present work was to correlate consumer panel acceptability versus trained sensory panel scores for appearance and flavor defects likely to appear during storage of whole milk powder. Descriptors selected for the study were: acid, caramel, cooked, dark color, lipolysis, and oxidized. For each descriptor a set of nine samples with different intensities were measured for acceptability and likelihood to consume by a 50-member consumer panel and for sensory intensity by a trained panel. Linear correlations between sensory acceptability and trained sensory panel scores were used to determine the sensory failure cut-off point for each descriptor, except caramel and cooked, which were not critical from the consumer's point of view. Differences in acceptability were found between Argentine and Uruguayan consumers for oxidized samples, while for lipolysis flavor, Argentine and Costa Rican consumers behaved similarly. For the color descriptor, significant changes in acceptability measured on a hedonic scale did not mean that consumers refused to consume the product. In contrast, for flavor descriptors, as soon as a significant decrease in acceptability occurred approximately 30% of the consumers said they would not consume the product. The sensory failure cut-off points presented in this paper can be used as a guide in future studies on the shelf life of MP and can also be of value in establishing sensory specifications for quality control programs. The methodology of correlating consumer acceptability to sensory panel scores and, thus, defining sensory failure is an improvement over more arbitrary criteria presented in most shelf-life studies.

A cell-free assay for detecting HDL that is dysfunctional in preventing the formation of or inactivating oxidized phospholipids.

We have developed a novel and rapid cell-free assay of the ability of HDL to prevent the formation of or inactivate oxidized phospholipids. HDL was tested for its ability to inhibit the oxidation of LDL, or inhibit the oxidation of l-alpha-1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine (PAPC) by hydroperoxyoctadecadienoic acid (HPODE), or inactivate oxidized PAPC (Ox-PAPC). In each case the fluorescent signal generated in the presence of the test substances and the test HDL was determined. As little as 2.5 microg of normal human HDL cholesterol significantly inhibited the fluorescent signal generated by Ox-PAPC; results did not differ regardless of whether the HDL was prepared by gel electrophoresis, fast protein liquid chromatography, or dextran sulfate precipitation. HDL from each of 27 patients with coronary atherosclerosis failed to inhibit the fluorescent signal generated by a control LDL, whereas HDL from each of 31 matched normal subjects with the same levels of HDL cholesterol significantly inhibited the signal. Results from an established cell-based assay (Navab, M., S. Hama, J. Cooke, G. M. Anantharamaiah, M. Chaddha, L. Jin, G. Subbanagounder, K. F. Faull, S. T. Reddy, N. E. Miller, and A. M. Fogelman. 2000. J. Lipid Res. 41: 1481-1494) were identical. HDL from the patients also failed to inhibit the fluorescent signal generated from PAPC plus HPODE (10 of 10 patients) whereas HDL from matched controls (8 of 8 patients) significantly inhibited the fluorescent signal. We conclude that this new assay has the potential to allow widespread testing of the hypothesis that HDL that is dysfunctional in preventing the formation or inactivating oxidized phospholipids may play an important role in the development of atherosclerosis.

Oxygenated carotenoid lutein and progression of early atherosclerosis: the Los Angeles atherosclerosis study.

BACKGROUND: Carotenoids are hypothesized to explain some of the protective effects of fruit and vegetable intake on risk of cardiovascular disease. The present study assessed the protective effects of the oxygenated carotenoid lutein against early atherosclerosis. EPIDEMIOLOGY: Progression of intima-media thickness (IMT) of the common carotid arteries over 18 months was determined ultrasonographically and was related to plasma lutein among a randomly sampled cohort of utility employees age 40 to 60 years (n=480). Coculture: The impact of lutein on monocyte response to artery wall cell modification of LDL was assessed in vitro by quantification of monocyte migration in a coculture model of human intima. Mouse models: The impact of lutein supplementation on atherosclerotic lesion formation was assessed in vivo by assigning apoE-null mice to chow or chow plus lutein (0.2% by weight) and LDL receptor-null mice to Western diet or Western diet plus lutein. IMT progression declined with increasing quintile of plasma lutein (P for trend=0.007, age-adjusted; P=0.0007, multivariate). Covariate-adjusted IMT progression (mean+/-SEM) was 0.021+/-0.005 mm in the lowest quintile of plasma lutein, whereas progression was blocked in the highest quintile (0.004+/-0.005 mm; P=0.01). In the coculture, pretreatment of cells with lutein inhibited LDL-induced migration in a dose-dependent manner (P<0.05). Finally, in the mouse models, lutein supplementation reduced lesion size 44% in apoE-null mice (P=0.009) and 43% in LDL receptor-null mice (P=0.02). CONCLUSIONS: These epidemiological, in vitro, and mouse model findings support the hypothesis that increased dietary intake of lutein is protective against the development of early atherosclerosis.

Mitogen-activated protein kinase phosphatase 1 activity is necessary for oxidized phospholipids to induce monocyte chemotactic activity in human aortic endothelial cells.

Entrapment and oxidation of low density lipoproteins (LDL) in the sub-endothelial space is a key process in the initiation of atherosclerotic lesion development. Functional changes induced by oxidized lipids in endothelial cells are early events in the pathogenesis of atherosclerosis. Oxidized-l-alpha-1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (ox-PAPC), a major component of minimally modified/oxidized-LDL (MM-LDL) mimics the biological activities assigned to MM-LDL both in vitro in a co-culture model as well as in vivo in mice. We hypothesized that ox-PAPC initiates gene expression changes in endothelial cells that result in enhanced endothelial/monocyte interactions. To analyze the gene expression changes that oxidized lipids induce in endothelial cells, we used a suppression subtractive hybridization procedure to compare mRNA from PAPC-treated human aortic endothelial cells (HAEC) with that of ox-PAPC-treated cells. We report here the identification of a gene, mitogen-activated protein kinase phosphatase 1 (MKP-1), that is rapidly and transiently induced in ox-PAPC-treated HAEC. Inhibition of MKP-1 using either the phosphatase inhibitor sodium orthovanadate or antisense oligonucleotides prevents the accumulation of monocyte chemotactic activity in ox-PAPC-treated HAEC supernatants. Furthermore, we show that decreased monocyte chemotactic activity in HAEC treated with sodium orthovanadate or MKP-1 antisense oligonucleotides is due to decreased MCP-1 protein. Our results implicate a direct role for MKP-1 in ox-PAPC-induced signaling pathways that result in the production of MCP-1 protein by ox-PAPC-treated HAEC.

Genetic control of HDL levels and composition in an interspecific mouse cross (CAST/Ei x C57BL/6J).

Strain CAST/Ei (CAST) mice exhibit unusually low levels of high density lipoproteins (HDL) as compared with most other strains of mice, including C57BL/6J (B6). This appears to be due in part to a functional deficiency of lecithin:cholesterol acyltransferase (LCAT). LCAT mRNA expression in CAST mice is normal, but the mice exhibit several characteristics consistent with functional deficiency. First, the activity and mass of LCAT in plasma and in HDL of CAST mice were reduced significantly. Second, the HDL of CAST mice were relatively poor in phospholipids and cholesteryl esters, but rich in free cholesterol and apolipoprotein A-I (apoA-I). Third, the adrenals of CAST mice were depleted of cholesteryl esters, a phenotype similar to that observed in LCAT- and acyl-CoA:cholesterol acyltransferase-deficient mice. Fourth, in common with LCAT-deficient mice, CAST mice contained triglyceride-rich lipoproteins with "panhandle"-like protrusions. To examine the genetic bases of these differences, we studied HDL lipid levels in an intercross between strain CAST and the common laboratory strain B6 on a low fat, chow diet as well as a high fat, atherogenic diet. HDL levels exhibited complex inheritance, as 12 quantitative trait loci with significant or suggestive likelihood of observed data scores were identified. Several of the loci occurred over plausible candidate genes and these were investigated. The results indicate that the functional LCAT deficiency is unlikely to be due to variations of the LCAT gene. Our results suggest that novel genes are likely to be important in the control of HDL metabolism, and they provide evidence of genetic factors influencing the interaction of LCAT with HDL.

Normal high density lipoprotein inhibits three steps in the formation of mildly oxidized low density lipoprotein: steps 2 and 3.

Treatment of human artery wall cells with apolipoprotein A-I (apoA-I), but not apoA-II, with an apoA-I peptide mimetic, or with high density lipoprotein (HDL), or paraoxonase, rendered the cells unable to oxidize low density lipoprotein (LDL). Human aortic wall cells were found to contain 12-lipoxygenase (12-LO) protein. Transfection of the cells with antisense to 12-LO (but not sense) eliminated the 12-LO protein and prevented LDL-induced monocyte chemotactic activity. Addition of 13(S)-hydroperoxyoctadecadienoic acid [13(S)-HPODE] and 15(S)-hydroperoxyeicosatetraenoic acid [15(S)-HPETE] dramatically enhanced the nonenzymatic oxidation of both 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (PAPC) and cholesteryl linoleate. On a molar basis 13(S)-HPODE and 15(S)-HPETE were approximately two orders of magnitude greater in potency than hydrogen peroxide in causing the formation of biologically active oxidized phospholipids (m/z 594, 610, and 828) from PAPC. Purified paraoxonase inhibited the biologic activity of these oxidized phospholipids. HDL from 10 of 10 normolipidemic patients with coronary artery disease, who were neither diabetic nor receiving hypolipidemic medications, failed to inhibit LDL oxidation by artery wall cells and failed to inhibit the biologic activity of oxidized PAPC, whereas HDL from 10 of 10 age- and sex-matched control subjects did. We conclude that a) mildly oxidized LDL is formed in three steps, one of which involves 12-LO and each of which can be inhibited by normal HDL, and b) HDL from at least some coronary artery disease patients with normal blood lipid levels is defective both in its ability to prevent LDL oxidation by artery wall cells and in its ability to inhibit the biologic activity of oxidized PAPC.

Short-term feeding of atherogenic diet to mice results in reduction of HDL and paraoxonase that may be mediated by an immune mechanism.

Short-term feeding (up to 7 days) of an atherogenic diet to C57BL/6 low density lipoprotein receptor-deficient mice did not result in decreased hepatic paraoxonase (PON) mRNA but caused a dramatic decrease in plasma PON activity and mass. The decreased activity and mass were temporally related to an increase in plasma and high density lipoprotein (HDL) lipid hydroperoxides and to a decrease in HDL cholesterol and native apolipoprotein A-I (apoA-I) and apolipoprotein A-II (apoA-II). As the native apoA-I protein disappeared from the circulation, higher molecular weight forms of apoA-I appeared, some of which contained epitopes recognized by an antibody (EO6) that recognizes oxidized phospholipids. After mice consumed an atherogenic diet for 1 or 3 days, switching the mice to a low fat chow diet for 3 days resulted in a return to baseline levels of lipid hydroperoxides but only a small return toward baseline for HDL cholesterol, with no significant increase in apoA-I mass or PON activity and mass. After mice consumed an atherogenic diet for 3 days, switching to the chow diet for 3 days did not significantly alter the high molecular weight forms of apoA-I or the signal generated by EO6. In marked contrast, after mice consumed an atherogenic diet for 7 days, switching to the chow diet for 3 days resulted in a dramatic increase in native apoA-I to baseline levels, with virtual disappearance of the high molecular weight forms of apoA-I, including the form recognized by EO6. After mice consumed an atherogenic diet for 7 days, switching to the chow diet for 3 days also resulted in significant increases in HDL cholesterol and PON mass and activity, although baseline levels were not reached. IgG and IgM antibodies were found to be associated with apoA-I in control animals, were minimally decreased after the 3-day atherogenic diet, were dramatically decreased after the 7-day atherogenic diet, and returned to near or above baseline levels after a return to the chow diet for 3 days. We conclude that the atherogenic diet rapidly induces lipid hydroperoxide formation and apoA-I oxidation with the formation of high molecular weight forms of apoA-I. Concomitant with these changes in apoA-I levels, HDL cholesterol and PON activity and mass declined without changes in mRNA levels for apoA-I or PON, suggesting increased clearance of these altered HDL particles. We further conclude that between the third and seventh day of the atherogenic diet, an as-yet-unidentified mechanism for clearing the high molecular weight forms of apoA-I is induced and that this mechanism may be related to the clearance of immune complexes.

High density associated enzymes: their role in vascular biology.

Enzymes associated with circulating HDL include lecithin: cholesterol acyl transferase, phospholipid transfer protein, cholesterol ester transfer protein, paraoxonase 1 and platelet activating factor acetylhydrolase. Together with lipoprotein lipase and hepatic lipase these enzymes produce important lipoprotein remodeling and modulate their structure and function and therefore their role in artery wall metabolism.

K-12 enrollment forecasting: merging methods and judgment.

"This article describes an enrollment forecasting process in which technical experts and local community stakeholders [in Oregon] worked together to produce data that were cost-efficient and yet accurate enough to serve as the basis for sound decisions. The large school district that employed this process gained valuable insights to guide its attendance zone and facilities planning decisions, and also created a group of key communicators to ensure community understanding and support."

Lie as narrative truth in abused adopted adolescents.

Two case examples of abused adopted adolescents are discussed to highlight tension within the treatment relationship when the therapist is expected to accept without question a clearly unbelievable story. These examples illustrate how the lies of such youths can function as narrative truth. The unbelievable tales that emerge in the therapeutic work effectively alter the adolescents' perceptions about the perplexing loss of continuity, both internal and external, that occurred when they were removed from their homes. Characters in the stories represent fragmented self- and object-representations as victim, abuser, rescuer, and passive onlooker. Counterparts to the patient as victim, abuser, rescuer, and passive onlooker can be recognized in the therapist's subjective responses. If the therapist can use countertransference to inform an understanding of the treatment process, an appreciation emerges that the truth of the lie is in its impact. Decisions about how to intervene can then be crafted. The second separation-individuation intrinsic to adolescent development is understood to provide a ripe opportunity for this working-through process.

A clinician with a family member with schizophrenia: a case report.

Clinicians who treat persons with schizophrenia often disagree with their patient's family about the etiology, treatment, and prognosis of the illness. Traditionally, such discrepancies have been a source of major tension and misunderstanding. The author reports a case that illustrates how a clinician, who herself had a family member with schizophrenia, became better able to bridge the gap in conceptual and empathic understanding that is often apparent between clinicians and families of schizophrenic patients. This clinician's personal views regarding the etiology, treatment, and prognosis of her schizophrenic family member are examined. Parallels are also drawn between the views of this clinician-family member and the current research on family acceptance patterns of the illness.

When confidentiality mandates a secret be kept: a case report.

The success of group psychotherapy is impeded when group members maintain secrets and fail to self-disclose to other group members. However, revealing secrets sometimes conflicts with the legal and ethical constraints of confidentiality, thus placing a greater burden on the group. The case reported here illustrates how complex the dynamics of group therapy become when one group member maintains a secret. In this case, one member maintained a secret about another to preserve that individual's right to privacy and confidentiality. This case also details the group member's deliberations and confusion about the effect his secret had on the group's success, as well as the burden he experienced by choosing to preserve confidentiality at the expense of successful therapy for himself.

Monocyte transmigration induced by modification of low density lipoprotein in cocultures of human aortic wall cells is due to induction of monocyte chemotactic protein 1 synthesis and is abolished by high density lipoprotein.

Incubation of cocultures of human aortic endothelial (HAEC) and smooth muscle cells (HASMC) with LDL in the presence of 5-10% human serum resulted in a 7.2-fold induction of mRNA for monocyte chemotactic protein 1 (MCP-1), a 2.5-fold increase in the levels of MCP-1 protein in the coculture supernatants, and a 7.1-fold increase in the transmigration of monocytes into the subendothelial space of the cocultures. Monocyte migration was inhibited by 91% by antibody to MCP-1. Media collected from the cocultures that had been incubated with LDL induced target endothelial cells (EC) to bind monocyte but not neutrophil-like cells. Media collected from cocultures that had been incubated with LDL-induced monocyte migration into the subendothelial space of other cocultures that had not been exposed to LDL. In contrast, media from separate cultures of EC or smooth muscle cells (SMC) containing equal number of EC or SMC compared to coculture and incubated with the same LDL did not induce monocyte migration when incubated with the target cocultures. High density lipoprotein HDL, when presented to cocultures together with LDL, reduced the increased monocyte transmigration by 91%. Virtually all of the HDL-mediated inhibition was accounted for by the HDL2 subfraction. HDL3 was essentially without effect. Apolipoprotein AI was also ineffective in preventing monocyte transmigration while phosphatidylcholine liposomes were as effective as HDL2 suggesting that lipid components of HDL2 may have been responsible for its action. Preincubating LDL with beta-carotene or with alpha-tocopherol did not reduce monocyte migration. However, pretreatment of LDL with probucol or pretreatment of the cocultures with probucol, beta-carotene, or alpha-tocopherol before the addition of LDL prevented the LDL-induced monocyte transmigration. Addition of HDL or probucol to LDL after the exposure to cocultures did not prevent the modified LDL from inducing monocyte transmigration in fresh cocultures. We conclude that cocultures of human aortic cells can modify LDL even in the presence of serum, resulting in the induction of MCP-1, and that HDL and antioxidants prevent the LDL induced monocyte transmigration.