Socially prescribed perfectionism predicts next-day binge eating behaviors over 20-days.

Existing research on perfectionism and binge eating suggests that socially prescribed, self-oriented, and other-oriented perfectionism (Socially Prescribed Perfectionism, SPP; Self-Oriented Perfectionism, SOP; and Other-Oriented Perfectionism, OOP) are differentially related to binge eating. However, previous studies have largely utilized cross-sectional methodology. The present study used a 20-day daily diary methodology to examine associations between daily levels of perfectionistic dimensions and next-day binge eating behaviors with a nonclinical sample of emerging adults (N = 263). Zero-inflated negative binomial regression models indicated that daily SPP (but not SOP or OOP) predicted a greater intensity of next-day binge eating behaviors in the count portion of the model; however, daily levels of perfectionistic dimensions did not predict the presence/absence of next-day binge eating behaviors in the zero-inflated portion of the model. Additionally, analyses examining the reverse causal direction (i.e., binge eating behaviors predicting higher next-day perfectionism) failed to provide evidence that the occurrence or intensity of binge eating behaviors predicts next-day levels of SPP, SOP, or OOP. Overall, at a daily level, SPP appears to be a vulnerability factor for binge eating behaviors. It may be helpful for clinicians to target state-levels of SPP to reduce harmful binge eating behaviors. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

CPB-assisted aortic valve replacement in a pregnant 27-year-old with endocarditis.

A 27-year-old, G(3)P( 2)A(0) female with acute Staph aureus (SA) endocarditis successfully underwent CPB-assisted aortic valve replacement with a bioprosthetic aortic valve at 22 weeks' gestation. This patient's presentation of acute endocarditis complicated by septic shock, congestive heart failure, severe aortic insufficiency, multiple septic embolic events and borderline renal failure appeared on the daunting background of chronic heavy tobacco usage, hepatitis C positivity, long-term IV drug abuse and a pregnancy into its twenty-second week. Optimal treatment strategies implemented for both mother and fetus throughout the perioperative period contributed to a successful outcome for both.

Outcomes comparison of 5 coated cardiopulmonary bypass circuits versus an uncoated control group of patients undergoing cardiac surgery.

UNLABELLED: Attenuated inflammatory response and decreased platelet activation have been claimed repeatedly when biocompatible circuits are used for cardiopulmonary bypass. We evaluated five Health Canada approved biocompatible circuit coatings (BCC) against an un-coated control group to determine their effectiveness in improving post-operative outcomes. Patients were assigned to the Control group or one of the 5 coated circuit groups: 40 Control; 33 Trillium; 32 Phisio; 34 Bioline; 33 X; and 11 GBS. Measured outcomes included: ventilator time; ICU time; post-operative chest tube drainage and transfusion volume; high sensitivity C-reactive protein (hsCRP); tau protein; and pre- and 72-hour post-operative anti-saccadic eye movement test comparisons. RESULTS: 183 patients were enlisted into the study. One arm of the study (GBS) was abandoned after 11 patients on account of inconsistent pressure excursions within the oxygenator and the excessive consumption of platelets necessitating transfusion. Patients in the X-coated group had significantly longer ventilator and intensive care unit (ICU) time compared to the three remaining coated circuit study groups. Though not significant, patients in the X group also demonstrated the highest post-operative chest tube losses, the most platelet transfusions, the highest tau protein levels and the lowest post-operative anti-saccadic eye movement test (ASEMT) results compared to the three remaining coated groups. The patients in the Trillium, Bioline and Phisio groups showed an improvement in ventilator and ICU time relative to the Control group. The diabetic patients in the Trillium, Bioline and Phisio groups showed an improvement in bleeding relative to the diabetic patients in the Control group. CONCLUSION: We compared all 5 coated circuits approved for clinical use in Canada against an uncoated control circuit. Three of the 5 coated circuits (Trillium, Phisio and Bioline BCC) were found to improve ventilator and ICU time compared to Control. Further studies are indicated to validate these results and their impact upon approval criteria, purchasing choices and safe clinical practice, especially as applied to higher risk diabetic patients.

Correlates of elevated blood pressure in healthy children: a systematic review.

The prevalence of hypertension in children is increasing globally. Addressing this will require a robust understanding of associated risk factors. To this end, we conducted a systematic review to identify correlates of elevated blood pressure (BP) in children. Literature searches were conducted using pre-defined search terms from three academic databases. The abstract and full text of identified studies were screened for eligibility by two independent reviewers. A total of 100 studies were included in this systematic review. An assessment tool was first used to assess study quality; a narrative synthesis was then performed. We found a broad range of physiological, social and behavioural factors associated with elevated BP in children. The most common correlate observed was adiposity, suggesting that childhood obesity may be implicated in the increased prevalence of hypertension observed in children. However, the broad range of other factors identified underscores the multi-factorial aetiology of hypertension. Data from a broad range of studies showed that the correlates of hypertension in children are multi-factorial. Therefore, approaches aimed at preventing hypertension must in turn be multi-factorial to ensure that the burden of hypertension in childhood is addressed.

Dysplasia Should Not Be Ignored in Lichenoid Mucositis.

Oral lichen planus is categorized as a potentially malignant condition by the World Health Organization; however, some argue that only lichen planus with dysplasia have malignant potential. Many pathologists call lichen planus with dysplasia "dysplasia with lichenoid mucositis (LM)" or "LM with dysplasia." Previous research has shown that certain high-risk patterns of loss of heterozygosity (LOH) in dysplastic lesions are associated with significantly increased cancer risk. However, LM without dysplasia lacks such molecular patterns, supporting the hypothesis that LM, by itself, is not potentially malignant and that only those with dysplasia have malignant potential. To further investigate the premalignant nature of LM with dysplasia, this study compared the rate of malignant progression of dysplasia with LM with that of dysplasia without LM. Patients from a population-based prospective cohort study with >10 y of follow-up were analyzed. Study eligibility included a histological diagnosis of a primary low-grade dysplasia with or without LM. A total of 446 lesions in 446 patients met the selection criteria; 373 (84%) were classified as dysplasia without LM, while 73 (16%) were classified as dysplasia with LM. Demographic and habit information, clinical information, and outcome (progression) were compared between the 2 groups. Forty-nine of 373 cases of dysplasia (13%) progressed compared to 8% (6/73) of dysplasia with LM. However, the difference was not statistically different ( P = 0.24). The 3- and 5-y rate of progression did not differ between the groups (6.7% and 12.5% for dysplasia without LM and 2.9% and 6.6% for those with LM; P = 0.36). Progression was associated with nonsmoking, location at a high-risk site, and diagnosis of moderate dysplasia regardless of whether LM was present or not. Dysplasia with or without LM had similar cancer risk, and dysplasia should not be discounted in the presence of LM.

Characterization of epithelial oral dysplasia in non-smokers: First steps towards precision medicine.

OBJECTIVES: Tobacco usage is the strongest risk factor in the development of oral squamous cell carcinoma (OSCC), which mandates careful screening for oral cancers in smokers. However, there are indications that oral potentially malignant lesions, such as oral epithelial dysplasia (OED), in non-smokers (NS) have a higher cancer risk than those in smokers. Without tobacco as an etiology, the development of these lesions in NS may suggest genetic susceptibility. The increasing incidence of OSCC in NS calls for a better understanding of the natural history of OED in NS as compared to that of smokers. MATERIALS AND METHODS: Patients from a population-based longitudinal study with more than 10 years of follow up were analyzed. Of the 455 patients with primary OED (233 mild and 212 moderate dysplasia), 139 were NS and 306 were smokers. Demographic and habit information, clinical information (lesion site, size and appearance; toluidine blue and fluorescent visualization), microsatellite analysis for loss of heterozygosity (LOH) and outcome (progression) were compared between the two groups. RESULTS AND CONCLUSIONS: The majority of patients with OED were smokers. Of these, more were males, non-Caucasians and heavy drinkers. A significantly higher number of OED in NS were in the tongue, whereas a significantly higher number of OED in smokers were in the floor of mouth (FOM). OED in NS showed a greater than 2-fold increase in cancer progression. Strikingly, OED located in the FOM in NS showed a 38-fold increase in cancer progression as compared to those in smokers.

Inhibitory effect of reducing agents on N-acetoxy- and N-hydroxy-2-acetylaminofluorene-induced mutagenesis.

The effect of cysteine (alpha-amino-beta-mercaptopropionic acid) on the mutagenic activities of the proximate carcinogen, N-hydroxy-2-acetylaminofluorene, and the ultimate carcinogen, N-acetoxy-2-acetylaminofluorene, was examined by estimating the frequency of his+ revertants of Salmonella typhimurium. Nontoxic concentrations of cysteine significantly reduced the formation of revertants when it was applied concurrently with the two carcinogens. Cysteine showed no detectable effect on mutagenesis when added to bacteria before or after exposure to carcinogens. The magnitude of inhibition of mutagenesis depended on the dose of cysteine and the concentration of the carcinogens. Cysteine at equimolar concentrations inhibited to a larger degree the mutagenesis induced by N-hydroxy-2-acetylaminofluorene than it inhibited that elicited by N-acetoxy-2-acetylaminofluorene. The inhibitory action of cysteamine and glutathione was comparable to that of cysteine. The results appear to be consistent with the assumption that cysteine traps electrophiles prior to their action on DNA.

Inflammation, chromosomal instability, and cancer: the schistosomiasis model.

Evidence is accumulating in support of a role for reactive oxygen species in the etiology of cancer. Inflammatory cells, such as neutrophils, macrophages, and eosinophils, are an important endogenous source of oxygen radicals. Stimulation of these cells by tumor promoters or by foreign bodies (parasites, bacteria, etc.) causes the release of reactive oxygen species. Laboratory studies have shown that genetic damage and neoplastic transformation are induced in vitro in cells cocultured with activated inflammatory cells. We have recently begun to study the role of inflammatory reactions in inducing genetic damage in a human population. This paper describes our initial studies of Egyptian patients infected with Schistosoma haematobium. This infection induces chronic inflammation and irritation in the urinary bladder and is associated with increased cancer at this site. We describe a recently completed population study that shows that infected individuals have elevated levels of genetic damage in their bladders, as measured by the exfoliated cell micronucleus test. Treatment that kills the parasite also reduces the micronucleus frequencies. We also explore the hypothesis that altered sensitivity of clones of cells in these patients to reactive oxygen species could be a force that drives the development of neoplasia by facilitating clonal expansion. Evidence is presented for the possible involvement of loci on chromosome 11 in controlling the level of chromosomal breakage caused by oxidative damage. We have shown that bladder carcinoma cells are sensitive to micronucleus induction by promoter-activated neutrophils and that they can be protected from this damage by insertion of a normal chromosome 11. Further work is in progress to define the source of chromosomal breakage in schistosomiasis patients and to begin to develop an understanding of the host factors protecting bladder cells in these individuals from genetic damage.

Elevation of interferon beta-inducible proteins in ataxia telangiectasia cells.

The recently cloned ATM gene has been shown to bear considerable homology to phosphatidylinositol 3 kinases and, therefore, its product may function in signal transduction. In this study, we report constitutively elevated levels of two IFN-beta-inducible proteins, ubiquitin cross-reactive protein (UCRP), and low molecular weight protein (LMP2), in human fibroblasts with the inherited disease ataxia telangiectasia (AT). Using immunoblotting, it was found that a M(r) 15,000 band representing free UCRP was hardly detectable in normal cells, while it was the predominant band in AT cells. Similarly, the expression of a M(r) 23,000 protein, LMP2 was found to be higher in AT cells than in normal cells. Culturing three successive passages of the AT cell line in the presence of different concentrations of neutralizing antibodies against IFN-beta caused partial and complete reduction, respectively, of the free UCRP and LMP2 signals to normal levels. These results indicate that UCRP and LMP2 pools may be basally elevated in AT cells due to constitutive activation of the IFN-beta induction pathway and are in keeping with the recently reported constitutive activation of the NF-kappaB transcriptional activator in AT cells.

Partial allelotype of carcinoma in situ of the human bladder.

Carcinoma in situ (CIS) of the urinary bladder is an aggressive lesion that frequently progresses to an invasive tumor, yet the underlying molecular changes in this lesion are largely unknown. In this study, we microdissected 31 cases of CIS and examined them for loss of heterozygosity (LOH) on 13 chromosomal arms. Twenty-nine microsatellite markers were chosen for this analysis based on their location in regions previously shown to be frequently lost in primary transitional cell carcinoma of the bladder. LOH of chromosome 9 was a frequent event in these samples, occurring in 77% of these lesions, with 19 of 31 cases showing deletion on the 9p arm (61%) and 17 of 28 cases displaying LOH on 9q (61%). Fine mapping at 9p21 demonstrated that CIS also displayed a high frequency of homozygous deletion surrounding the p16INK4A locus, like superficial papillary tumors, the other form of noninvasive lesion found in the bladder. However, loss of 14q (70%) was frequent in CIS yet extremely rare in papillary lesions (9%). Other chromosomal arms showing frequent LOH included 8p (65%), 17p (60%), 13q (56%), 11p (54%), and 4q (52%), whereas slightly lower frequencies of loss were observed for 11q (36%), 4p (32%), 3p (31%), 18q (29%), and 5q (20%). CIS lesions already possess many of the genetic alterations displayed by invasive transitional cell carcinomas, potentially accounting for the aggressive nature of these lesions.

The use of exfoliative cell samples to map clonal genetic alterations in the oral epithelium of high-risk patients.

Although it is widely accepted that clonal genetic alterations are an essential component of tumor progression, little is known of the distribution of such changes in high-risk lesions or how such clones are altered over time. We explored the feasibility of using exfoliative cells collected by scraping the mucosal surface to detect allelic loss in oral lesions of 22 patients (14 squamous cell carcinomas, 2 carcinomas in situ, and 6 dysplasias). The data show that the patterns of allelic loss observed in these samples closely represent those observed in biopsies of the same region. Furthermore, early indications are that this approach can be used to detect recurrent outgrowth of clones of altered cells in patients after therapy.

Use of allelic loss to predict malignant risk for low-grade oral epithelial dysplasia.

One of the best approaches to identifying genetic changes critical to oral cancer progression is to compare progressing and nonprogressing oral premalignant lesions. However, such samples are rare, and they require long-term follow-up. The current study used the large archive network and clinical database in British Columbia to study loss of heterozygosity (LOH) in cases of early oral premalignancies, comparing those with a history of progression to carcinoma in situ or invasive cancer and those without a history of progression (referred to as nonprogressing cases). Each of 116 cases was analyzed for LOH at 19 microsatellite loci on seven chromosome arms (3p, 4q, 8p, 9p, 11q, 13q, and 17p). The progressing and nonprogressing cases showed dramatically different LOH patterns of multiple allelic losses. An essential step for progression seems to involve LOH at 3p and/or 9p because virtually all progressing cases showed such loss. However, LOH at 3p and/or 9p also occurred in nonprogressing cases. Individuals with LOH at 3p and/or 9p but at no other arms exhibit only a slight increase of 3.8-fold in relative risk for developing cancer. In contrast, individuals with additional losses (on 4q, 8p, 11q, or 17p), which appeared uncommon in nonprogressing cases, showed 33-fold increases in relative cancer risk. In conclusion, analysis of LOH at 3p and 9p could serve as an initial screening for cancer risk of early premalignancies. Follow-up investigation for additional losses would be essential for predicting cancer progression.

Inhibition of spontaneous mutagenesis in yeast cultures by selenite, selenate and selenide.

Sodium selenite (1--15 mumol/plate) was found to completely suppress spontaneous mutagenesis at 2 independent loci in both wild (YO-300-IC) and mutator (mut 1-1, mut 2-2, mut 3-1, mut 4-1, mut 5-2, mut 6-1, mut 8-1, mut 9-1 and mut 10-1) isogenic strains of Saccharomyces cerevisiae. The 2 loci which where studied were his 1-7, a missense mutation, and lys 1-1, a super-suppressible mutant of the amber variety. The degree of suppression of spontaneous reversion to prototrophy at these 2 loci depended on the concentration of sodium selenite present, the strain of yeast being studied, and the loci being studied. Greater concentrations of sodium selenite (up to 30-fold higher) were required to suppress the frequency of spontaneous reversion at the histidine locus compared to quantities necessary to elicit a similar inhibition of lysine spontaneous reversion rates. The 2 loci also responded differently to the presence of 2 other inorganic selenium derivatives. Spontaneous mutagenesis at the lysine locus for strain YO-800-1C (mu 1-1) was completely inhibited by sodium selenide at 3 mumol/plate with complete suppression of histidine reversion occurring at 30 mumol/plate. Sodium selenate suppressed the spontaneous mutagenesis at the lysine, but not the histidine locus. These results indicate that environmentally added components can have a significant effect on the genetically controlled predisposition of an organism to mutagenesis and suggest the complexity of such interactions.

Micronuclei in exfoliated human cells as a tool for studies in cancer risk and cancer intervention.

The use of the micronucleus test on exfoliated cells as an approach to identify genotoxic damage in human tissues which are targets for organ-specific carcinogens and from which carcinomas will develop, is described. Chromosomal damage by carcinogens to dividing basal cells of the epithelium results in the production of micronuclei in the daughter cells which migrate up through the epithelium and are exfoliated. Exfoliated cells can be readily obtained from several tissues, including the oral buccal mucosa (scrapings of oral cells), bronchi (sputum), urinary bladder and ureter (centrifugation of urine), cervix (smears) and esophagus (imprints from biopsies). The micronucleus test on exfoliated cells has been successfully used to: (1) recognize population groups at an elevated risk for cancer of the oral cavity or urinary bladder; (2) estimate synergistic or additive effects of carcinogen exposure (cigarette smokers plus drinkers of alcoholic beverages); (3) pinpoint the site within an organ from which most carcinomas will develop (oral cancers among 'inverted' smokers in the Philippines). The possibility that this assay may also serve as a rapid monitor for chemopreventive agents is suggested by a preliminary trial on the effect of vitamin A/beta--carotene dietary supplementation among 33 betel quid chewers in the Philippines. These individuals received sealed capsules of retinol (100,000 IU/week) and beta-carotene (300,000 IU/week) for a 3-month period. At the end of this time, the frequencies of micronucleated buccal mucosa cells were reduced from an average of 4.2% to 1.4%. No changes were observed in micronucleus frequencies among 11 betel quid chewers not receiving vitamin pills. Non- chewers of betel quid in this population had a micronucleus frequency of 0.5%.

Response of fibroblast cultures from ataxia-telangiectasia patients to oxidative stress.

The object of this study was to determine whether ataxia-telangiectasia (AT) cells are more sensitive than normal cells to reduced oxygen species generated either during normal cell processes or resulting from metabolism of xenoblotics. To test this hypothesis four AT and four normal fibroblast cultures were exposed to hydrogen peroxide (H2O2) and the induction of micronucleated cells was assayed. AT cultures responded to the H2O2 treatment with a greater increase in micronucleus frequencies than that observed in normal cultures (P less than 0.01). At time course study showed that an elevation in micronucleus frequencies occurred earlier in AT cultures (significant increase by 1.5 h after treatment) than in normal cultures, possibly indicating a G2-phase sensitivity of AT cells to H2O2. The addition of an aqueous extract of areca nut to the cultures, as an example of exogenous stress, induced a greater frequency of micronucleated cells in AT cultures than in the normal cultures. These results suggest that the AT syndrome may serve as a model for investigating the role of reduced oxygen species in cancer.

Oral lesions, genotoxicity and nitrosamines in betel quid chewers with no obvious increase in oral cancer risk.

A link between the generation of areca nut-related N-nitrosamines in the saliva, the induction of genotoxic damage in the oral mucosa, as judged by an increase in micronucleated exfoliated cells (MEC), and a low incidence of oral cancer was studied in 2 population groups characterized by their habit of chewing quids without tobacco: Guamanians, who chew areca nuts (Areca catechu) with or without the addition of betel leaf (Piper betle); Taiwanese, who use areca nut, betel leaf or inference and slaked lime. The levels of N-nitrosoguvacoline (NG) in the saliva of chewers of fresh green areca nuts were very high (70.8 ng/ml) as compared to those reported for individuals using the more complex Indian betel quids (0.91 ng/ml or 5.6 ng/ml). None of the other areca nut-related nitrosamines (N-nitrosoguvacine (NGC), 3-(methylnitrosamino)propionitrile (MNPN) and 3-(methylnitrosamino)propionaldehyde (MNPA)) were detected in the saliva of Taiwanese betel quid chewers. The addition of slaked lime to the areca nut enhances the formation of NG during a chewing session. The frequency of MEC did not increase in the oral mucosa of areca nut chewers who do not use slaked lime, but showed a small but significant elevation in individuals using lime-containing quids. The elevation of MEC in Taiwanese, who are at low risk for oral cancer, is relatively small as compared to that found in chewers of Indian betel quids (pan), who show a highly elevated oral cancer risk. The results seem to suggest that NG may play only a minor role, if any, in the etiology of oral cancer among betel quid chewers.

Use of exfoliated cells to study tissue-specific levels of beta-carotene in humans.

This study was designed to explore the feasibility of using exfoliated cells to study beta-carotene incorporation into different epithelial tissues in humans. Exfoliated cells were collected from the oral cavities (by brushing the oral mucosa) and from the urogenital tracts (by centrifuging urine samples) of 36 females and basal levels of beta-carotene (without oral supplementation) were determined. Beta-carotene levels in cells from the two sites differed significantly, although a weak correlation was observed. As a second aspect of the study, 10 of these females were given oral supplementation with beta-carotene (90 mg twice weekly for 4 weeks). Beta-carotene levels increased significantly in both exfoliated urogenital tract (6.8-fold) and oral mucosa (5-fold) cells. However, the supplemented levels remained significantly different for the two types of cells. Beta-carotene levels did not change in individuals receiving a placebo treatment (n = 7). These studies suggest that exfoliated cells collected from different sites may be of value in quantifying tissue levels of beta-carotene during cancer intervention trials.

Localized induction of micronuclei in the oral mucosa of xeroderma pigmentosum patients.

Xeroderma pigmentosum (XP) patients are predisposed not only to skin cancers but also to tumors on the tip of the tongue. Although this enhanced risk has been attributed to a defect in the repair of DNA damage induced by ultraviolet rays from sunlight there is a lack of data showing that DNA damage is occurring in vivo at these sites. In order to determine whether a relationship exists between exposure to ultraviolet light and the level of chromosomal breakage occurring in epithelial tissue in XP patients, the exfoliated cell micronucleus test was applied to different sites in the oral cavities of four XP patients: the right and left buccal mucosa, the dorsal tip of the tongue and the palate. Six Egyptian controls were sampled concurrently. Micronucleus (MN) frequencies were higher in XP patients than in controls for all sites except the palate, where technical difficulties were encountered. In addition, an unequal distribution of the frequency of micronucleated cells was found in the different sample sites of the oral cavity in the XP patients, with the greatest elevation in frequencies among cells collected from the dorsal tip of the tongue. In contrast, the frequency of micronucleated cells did not vary significantly in samples from different sites obtained from the controls. These data suggest that the complex interplay of host and environmental factors can affect MN frequencies when this endpoint is used to quantify in vivo genotoxic damage in a tissue.

Clastogenic activity in urine of individuals with urinary bladder infections.

The object of this study was to determine whether an elevation in chromosome-damaging (clastogenic) activity occurred in the urine of individuals with bladder infections. Urine samples were collected from 18 patients with chronic (long-term) bladder infections (CBI). Organic material was extracted from urine by preparative reversed-phase high-pressure liquid chromatography and assayed for chromosome-damaging activity in Chinese Hamster Ovary (CHO) cell cultures. Clastogenic activity was present in these urine extracts at levels significantly above those observed in control individuals (P less than 0.001). These levels were comparable to those observed in smoker's urine. In addition, 2 of 4 individuals with acute (short-term) bladder infection (ABI) showed a significant elevation in clastogenic activity in their urine samples (P = 0.025). This study indicates that clastogenic components can be produced during bacterial infections in the urinary bladder and supports a direct involvement of urinary tract infections in the development of bladder cancer.

Mutagenic activity of ascorbate in mammalian cell cultures.

Exposure of Chinese hamster ovary (CHO) cells to solutions of ascorbate (2--5 x 10(-4) M) resulted in the induction of somatic mutations at the hypoxanthineguanine phosphoribosyl transferase (HGPRT) locus. Mutant cells were resistant to 6-thioguanine (10 microgram/ml) and sensitive to HAT (hypoxanthine, aminopterin, thymidine) medium. Doses of ascorbate which were mutagenic were also toxic. Addition of catalase to such ascorbate concentrations prevented both mutagenesis and toxicity. This suggests that mutagenic metabolites of ascorbate may involve peroxide radicals.