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Biomedical subjects

J S Hayes

Publications and source records attributed to J S Hayes.

At least 19 recordsLinked to original sources
PubMed2005

Determination of 5-log pathogen reduction times for heat-processed, acidified vegetable brines.

Recent outbreaks of acid-resistant food pathogens in acid foods, including apple cider and orange juice, have raised concerns about the safety of acidified vegetable products. We determined pasteurization times and temperatures needed to assure a 5-log reduction in the numbers of Escherichia coli O157:H7, Listeria monocytogenes, and Salmonella strains in acidified cucumber pickle brines. Cocktails of five strains of each pathogen were (separately) used for heat-inactivation studies between 50 and 60 degrees C in brines that had an equilibrated pH value of 4.1. Salmonella strains were found to be less heat resistant than E. coli O157:H7 or L. monocytogenes strains. The nonlinear killing curves generated during these studies were modeled using a Weibull function. We found no significant difference in the heat-killing data for E. coli O157:H7 and L. monocytogenes (P = 0.9709). The predicted 5-log reduction times for E. coli O157:H7 and L. monocytogenes were found to fit an exponential decay function. These data were used to estimate minimum pasteurization times and temperatures needed to ensure safe processing of acidified pickle products and show that current industry pasteurization practices offer a significant margin of safety.

Adaptation, Physiological↗
PubMed2004

Independent effects of acetic acid and pH on survival of Escherichia coli in simulated acidified pickle products.

Our objective was to determine the effects of organic acids and pH on the rate at which selected strains of Escherichia coli O157:H7 die in acid solutions representative of acidified pickle products (pH < 4.6). We used gluconic acid/sodium gluconate (pKa = 3.7) as a noninhibitory buffer to maintain pH at selected values in the absence of other organic acids. This was possible because we found that the inhibitory effects of this acid on E. coli strains at pH 3.1 were independent of acid concentration over a range of 2 to 200 mM. By this method, the lethal effects of acetic acid solutions (100 to 400 mM) at selected pH values between 3.1 and 4.1 were compared with the effects of pH alone (as determined using gluconate buffer). We found D-values were two- to fourfold lower with acetic acid compared with the effect of pH alone for simulated pickle brines in this pH range. Glutamic acid, an amino acid that is known to enhance acid resistance in E. coli and is a component of pickle brines, protected the E. coli strains from the specific effects of acetic acid.

Acetic Acid↗
PubMed1999

The prostacyclin receptor is isoprenylated. Isoprenylation is required for efficient receptor-effector coupling.

The prostacyclin receptor (IP), a G protein-coupled receptor, mediates the actions of the prostanoid prostacyclin and its mimetics. IPs from a number of species each contain identically conserved putative isoprenylation CAAX motifs, each with the sequence CSLC. Metabolic labeling of human embryonic kidney (HEK) 293 cells stably overexpressing the hemagluttinin epitope-tagged IP in the presence of [(3)H]mevalonolactone established that the mouse IP is isoprenylated. Studies involving in vitro assays confirmed that recombinant forms of the human and mouse IP are modified by carbon 15 farnesyl isoprenoids. Disruption of isoprenylation, by site-directed mutagenesis of Cys(414) to Ser(414), within the CAAX motif, abolished isoprenylation of IP(SSLC) both in vitro and in transfected cells. Scatchard analysis of the wild type (IP) and mutant (IP(SSLC)) receptor confirmed that each receptor exhibited high and low affinity binding sites for [(3)H]iloprost, which were not influenced by receptor isoprenylation. Whereas stable cell lines overexpressing IP generated significant agonist (iloprost and cicaprost)-mediated increases in cAMP relative to nontransfected cells, cAMP generation by IP(SSLC) cells was not significantly different from the control, nontransfected HEK 293 cells. Moreover, co-expression of the alpha (alpha) subunit of Gs generated significant augmentations in cAMP by IP but not by IP(SSLC) cells. Whereas IP also demonstrated significant, dose-dependent increases in [Ca(2+)](i) in response to iloprost or cicaprost compared with the nontransfected HEK 293 cells, mobilization of [Ca(2+)](i) by IP(SSLC) was significantly impaired. Co-transfection of cells with either Galpha(q) or Galpha(11) resulted in significant augmentation of agonist-mediated [Ca(2+)](i) mobilization by IP cells but not by IP(SSLC) cells or by the control, HEK 293 cells. In addition, inhibition of isoprenylation by lovastatin treatment significantly reduced agonist-mediated cAMP generation by IP in comparison to the nonisoprenylated beta(2) adrenergic receptor or nontreated cells. Hence, isoprenylation of IP does not influence ligand binding but is required for efficient coupling to the effectors adenylyl cyclase and phospholipase C.

Adenylyl Cyclases↗
PubMed1999

Florida's bicycle helmet law and a bicycle safety educational program: did they help?

INTRODUCTION: This research studied the effectiveness of Florida's mandatory helmet law for children and a community bicycle safety campaign promoting helmet use. Children's use of helmets before and after the law's enactment and the type and extent of head injuries sustained in bicycle crashes were evaluated. METHODS: The trauma and medical records from Broward General Medical Center's Pediatric Referral Trauma Center provided demographic data, injury severity scores, and information on the type and extent of head injuries sustained. Data were compared using independent sample t tests and Pearson chi(2) statistics with.05 as the significance level. RESULTS: Each group consisted of 72 children, predominantly 7- to 12-year-old boys. Known helmet use rose from 5.6% to 20.8%, with children aged 10 to 12 years having the greatest increase in helmet use (27%). Helmet use rose in urban and suburban areas. Changes in the type and extent of head injuries were mixed. Injury severity scores were higher for nonhelmeted children in the after-law group. DISCUSSION: Although helmet use increased, especially among the 7- to 12-year-olds targeted during the bicycle safety campaigns, bicycle helmet use remains too low, and nonhelmeted children continue to have a higher risk for serious injuries. Community bicycle safety programs that promote helmet use remain an important adjunct to mandatory helmet use laws.

Attitude to Health↗
PubMed1999

Nurses' perceptions: when is it a medication error?

This study investigates nurses' perceptions of medication errors and appropriate reporting. Results of the study suggest that nurses may not report because of fear of reprisal. Further, there may be a need to allow for nursing judgment in some instances; at those time, the term "medication error" may not be the most appropriate. Implications for nursing administration include further exploration of nonpunitive processes in response to adverse drug events.

Adult↗
PubMed1998

Malingering detection in a mentally retarded forensic population.

Thirty-nine patients in a forensic mental hospital were evaluated using the Structured Interview of Reported Symptoms (SIRS) and several tests used for detecting malingered psychiatric and neuropsychological dysfunction. Patients were initially classified by a multidisciplinary team as nonmalingering participants (n = 12) and known malingerers (n = 9). All participants in both groups were pretrial and had been found incompetent to stand trial by the court. Eighteen more patients found to be not guilty by reason of insanity by the courts were included in the study. Using the SIRS alone, 95% overall classification accuracy was obtained. When the scores on the Dot Counting Test, Memory for Fifteen Items Test, and the M-Test were added to the discriminant function, all patients were correctly classified to the respective groups. The results are discussed in terms of complimenting interdisciplinary team diagnosis with psychological tests for malingering.

Journal Article↗
PubMed1996

Differential vulnerability between postconcussion self-report and objective malingering tests in identifying simulated mild head injury.

The present study examined the ability of analog malingerers to feign postconcussion symptoms and neuropsychological performance patterns seen in mild head-injured patients. Experimental subjects were randomly assigned to either a control condition, asked to feign deficits consistent with mild head injury without task specific instruction, or feign deficits while given task-specific instruction. A separate group of mild head-injured patients served as a clinical comparison group. Analog malingering groups accurately simulated levels of postconcussive symptoms seen in the mild head-injured patients. However, poorer performance was displayed by the analog malingerers on the objective malingering tests. Coaching did not facilitate realistic patterns of performance for analog malingerers. The results of this study indicate that analog malingerers accurately replicated self-reported postconcussive symptoms, but were less able to simulate objective clinical malingering test performance. These results suggest that self-report measures of postconcussive symptoms and clinical tests are differentially vulnerable to simulation attempts.

Adolescent↗
PubMed1996

Enhanced antitumor efficacy of cisplatin in combination with ALRT1057 (9-cis retinoic acid) in human oral squamous carcinoma xenografts in nude mice.

Cisplatin (DDP) is commonly used to treat head and neck tumors. Therapy frequently fails due to development of DDP resistance or toxicities associated with DDP therapy. In this study, effects of ALRT1057 [9-cis retinoic acid (9-cis RA)] on DDP cytotoxicity were studied in a human oral squamous carcinoma xenograft model. Mice bearing xenografts were dosed p.o. daily 5 days/week with 30 mg/kg 9-cis RA and/or i.p. twice weekly with 0.3-0.9 mg/kg DDP. Maximum tolerated doses of 9-cis RA and DDP were approximately 60 and >/=2.9 mg/kg, respectively, under their dosing schedules and routes of administration. Control tumors grew rapidly with mean doubling times of 4 +/- 1 days and reached mean volumes of 1982 +/- 199 (SE) mm3 after 24 days. DDP at doses of 0.3, 0.45, and 0.9 mg/kg inhibited tumor growth by 28, 47, and 86%, respectively, 24 days after tumor cell implantation. Thirty mg/kg 9-cis RA inhibited tumor growth by 25%. In combination, 0.3 mg/kg DDP + 30 mg/kg 9-cis RA inhibited tumor growth by 68%; 0.45 mg/kg DDP + 30 mg/kg 9-cis RA inhibited growth by 78%. These decreases were greater than those that would have been produced by either agent summed separately. Of importance, at doses of 9-cis RA that enhanced DDP cytotoxicity, no change in dose tolerance was observed as compared to tolerances observed for either agent alone, indicating that 9-cis RA increased sensitivity to DDP without altering systemic toxicity. In addition, 9-cis RA profoundly altered squamous cell carcinoma phenotypes by suppressing squamous cell differentiation, resulting in tumors with increased numbers of basal cells. In contrast, DDP selectively depleted proliferating basal cells from carcinomas. In combination, morphological changes produced by 9-cis RA alone predominated, suggesting a possible basis for enhanced DDP sensitivity in tumors exposed to both agents. These data demonstrate that 9-cis RA enhances tumor sensitivity to DDP, and suggest that this combination should be tested in Phase I-II clinical trials for its potential for improving anticancer therapy of squamous cell cancers.

Alitretinoin↗
PubMed1995

Retinoid-induced suppression of squamous cell differentiation in human oral squamous cell carcinoma xenografts (line 1483) in athymic nude mice.

Retinoids are promising agents for therapy of squamous cancers. In vitro, retinoids decrease expression of differentiation markers in head and neck squamous carcinoma cells. Little information is available on effects of retinoids on head and neck squamous carcinoma cell xenograft growth in vivo. To address this issue, head and neck squamous carcinoma cells (line 1483) were established as xenografts in nude mice. Control tumors grew rapidly with doubling times of 4-6 days to mean volumes of 1696 mm3 after 24 days. Histological analyses indicated the formation of well-differentiated squamous carcinoma cells exhibiting pronounced stratification (basal and suprabasal cells) and keratinization (keratin pearls) with abundant stroma. Cytokeratin 19 expression was restricted to the basal cell layers, and cytokeratin 4 expression was abundant in suprabasal cells. Mice were treated daily with 30 mg/kg 9-cis retinoic acid, 20 mg/kg all-trans-retinoic acid, or 60 mg/kg 13-cis retinoic acid by p.o. gavage on a schedule of 5 days/week over 4 weeks. Low micromolar (1.48-3.67 microM) and nanomolar (200-490 nM) concentrations of 9-cis retinoic acid and all-trans-retinoic acid were measured in plasmas and xenografts, respectively, 30 min after dosing. Retinoid treatment produced a marked suppression of the squamous cell differentiation of tumor cells manifest by decreased keratinization, loss of stratification, and accumulation of basal cells. This was accompanied by large decreases in the number of CK4-positive cells and concomitant increases of CK19-positive cells. REtinoic acid receptor-beta expression was also increased by 2.9-9.7-fold after chronic retinoid treatment. 9-cis retinoic acid and all-trans-retinoic acid decreased tumor volumes by 23 +/- 5 (SE) and 19 +/- 3%, respectively (P < or = 0.05); 13-cis retinoic acid was inactive. These retinoids did not decrease the rate of exponential tumor growth but increased the latent period until exponential growth began. These studies demonstrate that retinoids do not universally decrease tumor growth but profoundly suppress squamous cell differentiation in vivo in this xenograft model.

Animals↗
PubMed1995

Specific interactions of progestins and anti-progestins with progesterone antibodies, plasma binding proteins and the human recombinant receptor.

This structure-activity study compares the affinity of a series of progestins, progesterone metabolites and anti-progestins for a panel of monoclonal antibodies to progesterone, coypu (Myocastor coypus) or guinea pig plasma progesterone-binding proteins (PPBPs) and the human recombinant progesterone receptor A form (PR-A). The compounds tested were progesterone, Promegestone (R5020), Mifepristone (RU486), ZK98,734, Onapristone (ZK98,299), 11 alpha-hydroxyprogesterone, 11 alpha-progesterone hemisuccinate, androsterone, etiocholanolone, 5 alpha- and 5 beta-pregnane-3,20-diones, and 20 alpha- and 20 beta-hydroxyprogesterones. The Ki values for these ligands were determined by competitive binding assays using radiolabelled progesterone as the binding site ligand. For anti-progesterone antibodies (e.g. DB3 and 11/32), only progesterone (3.6-8.8 nM), the 11 alpha-derivatives (1.0-5.5 nM) used to prepare the immunogen and the two 5-pregnanediones (20.9-45.1 nM) were bound with high affinity. For PR-A, high affinity binding was found with receptor agonists (Ki = 1.1-6.2 nM), both 5- and 20-reduced metabolites, and antagonists (0.6-28.0 nM), but not with the 11 alpha-derivatives (950 nM-1.0 microM). In contrast, the PPBPs displayed high affinity interactions with progesterone (3.5-4.2 nM) and both 5 alpha- and 20 alpha-reduced metabolites (2.4-3.4 nM). Binding with the beta-isomers and R5020 was less pronounced (22-170 nM) and there was no evidence of high affinity binding with PR antagonists (> 1.0 microM). Analogs with the 17-keto group did not bind to any of the binders studied. Thus, commonalities among the three types of protein binders were their comparable binding affinities for progesterone (3.5-8.8 nM) and 5-pregnanedione isomers (2.4-330 nM), and a lack of binding for two C17-keto steroids (androsterone and etiocholanolone). The results imply that the tertiary features of the binding domain of these three types of proteins are sufficiently different to result in unique binding structures.

Animals↗
PubMed1995

Phenylalanine-stimulated secretion of cholecystokinin is calcium dependent.

The secretion of cholecystokinin was examined in STC-1 cells, an intestinal cholecystokinin (CCK)-secreting cell line. Exposure to the amino acid L-phenylalanine increased release of CCK by 135%, 180%, and 251% of control levels after 15-min treatments with 5, 20, and 50 mM phenylalanine, respectively. L-Phenylalanine-induced secretion of CCK was inhibited by the calcium channel blocker diltiazem (10 microM). L-Phenylalanine (20 mM) also significantly increased cytosolic calcium levels in fura 2-acetoxymethyl ester (fura 2-AM)-loaded cells, and this increase was diltiazem sensitive. D-Phenylalanine, over the dose range of 5-50 mM, produced nonsignificant increases in CCK release. Treatment of STC-1 cells with 300 ng/ml of pertussis toxin for either 4 or 24 h did not significantly affect either basal release of CCK or L-phenylalanine-stimulated secretion. Patch-clamp recordings from cell-attached membrane patches showed a stimulation in calcium channel activity after L-phenylalanine. These results indicate that, in STC-1 cells, L-phenylalanine stimulates release of cholecystokinin via a calcium-dependent process.

Animals↗
PubMed1995

Influence of prior knowledge and experience on the ability to feign mild head injury symptoms in head injured and non-head-injured college students.

The present study investigated the effects of personal knowledge, experience and beliefs about traumatic brain injury (TBI) on persons' ability to successfully feign neuropsychological impairment. Head-injured and non-injured subjects completed the Head Injury Misconception Survey, and were evenly divided into malingering or control (do best) conditions. Subjects were given a scenario which asked them to imagine that they had been in a prior accident and were involved in litigation. They were then asked to either malinger or respond in the best way possible to a battery of neuropsychological tests. While instructions to malinger had a pronounced effect, knowledge of brain injury did not significantly influence an individual's ability to feign neuropsychological impairment. Future directions in the study of malingering are also discussed.

Journal Article↗
PubMed1995

Progesterone and oestrogen receptors in the decidualized mouse uterus and effects of different types of anti-progesterone treatment.

Pseudopregnant mice were treated systemically with monoclonal anti-progesterone antibody (DB3) (model 1), or progesterone receptor antagonists RU486 or ZK98,299 (ZK299) (model 2) on day 3 post coitum. On day 4, sesame oil was administered intraluminally into one uterine horn to induce decidualization. On day 7, the average mass of the oil-injected horn was 335.2 +/- 52.4 mg, eight times greater than that of the non-injected horn (40.8 +/- 5.3 mg; P < 0.001). After treatment with DB3, RU486 or ZK299, the masses of the injected horns did not differ significantly from those of non-injected horns. In the control group, concentrations of progesterone receptors (ligand-binding assay) increased twofold in the decidualized (52.2 +/- 7.4 fmol mg-1) compared with the non-injected horn (26.0 +/- 7.6 fmol mg-1; P < 0.05), whereas oestrogen receptor content (ligand-exchange assay) decreased by 53% (104.9 +/- 18.2 versus 224.3 +/- 18.1 fmol mg-1; P < 0.001). In model 1, antibody-treated animals showed a tenfold increase in the concentration of progesterone receptors (261.7 +/- 81.1 fmol mg-1; P < 0.001), but there was no differential distribution of progesterone or oestrogen receptors in the oil-injected versus non-injected uterine horns. In model 2, uterine progesterone and oestrogen receptors again showed no differential response between injected and non-injected horns regardless of the route of administration (systemic or intraluminal). Concentrations of progesterone receptors in RU486-treated (35.8 +/- 9.4 fmol mg-1) and ZK299-treated (32.0 +/- 10.2 fmol mg-1) mice were comparable to those in non-injected horns (35.3 +/- 6.3 and 34.2 +/- 5.1 fmol mg-1, respectively) and were not significantly different from the control group (26.0 +/- 7.6 fmol mg-1). The results show that oil-induced decidualization is accompanied by increased concentrations of progesterone receptors and decreased concentrations of oestrogen receptors. When decidualization is blocked by anti-progesterone treatment (antibody against progesterone or progesterone receptor antagonist), there are differing effects on receptor responses with an increase in progesterone receptors and decrease in oestrogen receptors after passive immunization, and no change in progesterone receptors and a reduction in oestrogen receptors after anti-progestins. The anti-decidualization effect in the two models was therefore achieved via dissimilar uterine receptor responses.

Animals↗
PubMed1995

Anti-progesterone antibody administration and the impairment of postpartum maternal care in mice.

Passive transfer of a monoclonal antibody against progesterone produces a high incidence of maternal rejection in mice after recovery from antibody-induced infertility. To investigate the mechanisms involved in this reduction of maternal care, we have examined whether the effect is due to long-term exposure to antibody. Antibody was administered i.p. either on day 2 or day 17 of pregnancy. When a low dose (1.0 nmol) was given on day 2, pregnancy proceeded normally but 44.8% pups delivered at term were rejected compared with 12.7% in the control group. When a higher dose (4.5 nmol) of antibody was given on day 17, pregnancy continued normally to term and the rejection rate was 48.8% (control: 11.1%). When the same amount of antibody was injected after delivery (day 1 of lactation), no detrimental effect was found on subsequent maternal care to the young, the rejection rate being comparable between antibody-treated and control groups (5.3% vs 4.6%). To determine if the presence of antibody interfered with lactation or suckling, a bolus injection of 10 microCi [3H]H2O was given to mice treated at day 17 with antibody or saline. The levels of radioactivity present in both mothers and pups and the first 5-day pup growth curves showed identical patterns, indicating that milk availability and the suckling process were not affected. Crossfostering studies revealed that antibody-treated mothers rejected 25.5% of fostered pups compared with 8.5% found in the control females when antibody was administered on day 17 of pregnancy and the entire litters were crossfostered between the two groups immediately after delivery.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Aberrant maternal behaviour in mice treated with a progesterone receptor antagonist during pregnancy.

The rapid onset of normal maternal behaviour after parturition in mice, consisting of cleaning, warming, feeding and protection of offspring, is primed by oestrogen, progesterone and oxytocin. Previous studies showed that passive transfer of monoclonal antibodies against progesterone significantly increases the incidence of maternal rejection of pups. To test the hypothesis that aberrant maternal behaviour is due to partial progesterone withdrawal leading to hormonal imbalance during late pregnancy, maternal rejection was assessed following treatment with a progesterone receptor antagonist. Mifepristone (RU486) was given subcutaneously on either day 2 (100 micrograms) or day 17 (50 micrograms) of pregnancy, or on the first day of lactation (100 micrograms). Maternal behaviour was monitored twice daily for the first 6 days of lactation and pup rejection recorded for a further 15 days. Maternal rejection was significantly greater after mifepristone administration on either day 2 or day 17 (28.6% and 38.3%) compared with controls (11.1% and 5.2% respectively). Rejection was negligible in both treated and control groups if mifepristone was given after parturition. When mothers were treated at day 17, the length of the latent period before pups were retrieved and returned to the nest was markedly increased in mifepristone-treated mothers (46.3 s) compared with controls (4.4 s) though the effect was transient. The results indicate that mifepristone interferes with the hormonal priming mechanism(s) necessary for the onset of normal maternal behaviour by a receptor-mediated effect. The similarity of the present results and those obtained with anti-progesterone antibodies implies that receptor antagonism or antibody scavenging of progesterone influence a common central nervous mechanism that is essential for the normal priming process.

Animals↗