Medical errors and medical culture. Changing the culture of blame requires a revolution.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to B Harrington.
Explore the source record for details and available documents.
Most local health departments utilize visual, but not microbiological, methods when inspecting food service operations. To evaluate the marginal utility of microbial testing for minimizing potential risks of foodborne outbreaks in restaurants, swab samples were taken from handwashing sink faucets, freshly cleaned and sanitized food-contact surfaces, and from cooler or freezer door handles in 70 of 350 category-three (high-risk) food service operations in Toledo, Ohio. The swabs were inoculated onto different selective media, and standard procedures were used to identify pathogenic and nonpathogenic bacteria. Microbiological evaluations of the sampled food service operations were compared with visual inspection reports, using a numeric rating scale. Enteric bacteria (that may indicate fecal contamination) were found on food contact surfaces, on cooler or freezer door handles, and on handwashing sink faucets in 86, 57, and 53% of the food service operations, respectively. Approximately 27, 40, and 33% of the restaurants received visual ratings of very poor to poor, fair, and good to very good, respectively. In comparison, 10, 17, and 73% of the restaurants received microbiological rating scores of very poor to poor, fair, and good to very good, respectively. Restaurants with trained personnel received significantly higher visual rating scores than restaurants without trained personnel (P < 0.01). Although more restaurants received poor rating scores by visual inspection than by microbiological evaluation, the presence of fecal bacteria from different sites in more than 50% of the food service operations indicated that visual inspection alone might not be sufficient for minimizing potential risk for foodborne disease outbreaks. Therefore, we recommend periodic microbiological evaluation of high-risk food service operations, in addition to visual inspection, for minimizing the risk of foodborne disease outbreaks.
Explore the source record for details and available documents.
Parkinson's disease is a neurodegenerative disease that is consequent to the loss of brain dopamine (DA) cells. These abnormalities are thought, in part, to be a manifestation of increased free radical production during the metabolism of catecholamines. The antiapoptic agent, bcl-2, has been shown to protect cells against the toxic effects of reactive oxygen species (ROS). Thus, we tested whether bcl-2 could attenuate the toxic effects of DA on immortalized neural cells. Our results show that DA caused dose-dependent cell death. The use of confocal microscopy and flow cytometry demonstrated that DA caused cell death through an apoptotic process. Moreover, DA caused a marked increase in ROS in these cells. Furthermore, overexpression of bcl-2 caused significant protection against DA-induced apoptosis. These results are discussed in terms of their support for a role of bcl-2 in the development of Parkinson's disease.
Explore the source record for details and available documents.
Fetal growth and development is dependent on the transfer of amino acids from maternal to fetal blood across the microvillous plasma membrane (MVM) and basal plasma membrane of placental syncytiotrophoblast. The aim of this study was to determine the relationship of system A amino acid transporter (SysA) activity in MVM to a variety of measurements of size at birth in a group of term small for gestational age (SGA) babies and in a group of appropriate for gestational age (AGA) babies. Mean SysA activities (nmol/mg vesicle protein/30 s +/- SEM) were: SGA, 0.027 +/- 0.004 (n = 25) and AGA, 0.045 +/- 0.005 (n = 24); p = 0.006. Spearman rank correlations were calculated for SGA (n = 19-25) and AGA (n = 21-24) groups for SysA activity against the following anthropometric measurements: abdominal circumference, birth weight, length, midarm circumference (MAC), head circumference, midarm circumference:head circumference ratio, placental weight (PW), placental ratio (placental weight:birth weight), birth weight:length ratio, Ponderal index (birth weight/length3) and triceps and subscapular skin-fold thicknesses (tsft and ssft). In SGA babies, SysA activity was positively correlated (p < 0.05) with subscapular skin-fold thicknesses (r = 0.48), triceps skin-fold thicknesses (r = 0.42), PW (r = 0.42), and placental ratio (r = 0.46). In AGA babies, the only significant correlation was an inverse one with placental ratio (r = -0.50). These data suggest there are differences in the relationship between placental SysA activity and fetal proportion in term AGA compared with SGA babies.
Cyclic vomiting syndrome is characterized by sudden episodes of vomiting and abdominal pain. It occurs primarily in children, is exacerbated by stress, and is often considered a migraine equivalent. Migraines have been linked to mast cells, which are often found close to neurons where they are activated by neuropeptides. We investigated the ultrastructural appearance of rat ileal brush border and mast cells following acute stress by immobilization. The effect of sulfated proteoglycans heparin and chondroitin sulfate was also tested on mast cell histamine secretion. Ileal brush border appeared intact in control animals, but was shorter and exhibited intercellular gaps after 30 min of acute immobilization stress. Mast cell activation in control rats was minimal, while stress induced obvious signs of activation as judged from disappearance of secretory granule electron dense contents. However, these intragranular changes were not accompanied by typical degranulation through exocytosis. Treatment of purified homogeneic rat peritoneal mast cells with 10(-4) M heparin or chondroitin sulfate 30 min prior to stimulation with 0.5 microg/ml compound 48/80 decreased histamine release by over 70% and 50% (P < 0.05), respectively. These results suggest the possible usefulness of chondroitin sulfate in conditions such as cyclic vomiting syndrome.
Explore the source record for details and available documents.
The discovery and characterisation of a novel species of Candida, termed Candida dubliniensis, associated with oral candidosis in HIV-infected individuals is described. These organisms share several phenotypic characteristics in common with Candida albicans and Candida stellatoidea, including the ability to produce germ tubes and chlamydospores. However, in contrast to these latter two species, C. dubliniensis isolates produce abundant chlamydospores, which are often arranged in contiguous pairs, triplets and other multiples suspended from a single suspensor cell. They belong to C. albicans serotype A and exhibit atypical substrate assimilation profiles. Genomic DNA fingerprinting analysis with the C. albicans-specific probe 27A and five different oligonucleotide probes consisting of short repeat sequence-containing motifs, demonstrated that C. dubliniensis has a distinct genomic organisation relative to C. albicans and C. stellatoidea. This was confirmed by karyotype analysis and random amplified polymorphic DNA (RAPD) analysis. Comparison of 500 bp of the V3 variable region of the large ribosomal subunit genes from 14 separate C. dubliniensis isolates and the corresponding sequences from C. albicans, C. stellatoidea, C. tropicalis, C. glabrata, C. parapsilosis, C. kefyr and C. krusei demonstrated that the C. dubliniensis isolates formed a homogenous cluster (100% similarity), representing a discrete taxon within the genus Candida that was significantly different from the other species analysed.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
After 30 days of streptozotocin-induced diabetes, the small intestine from untreated diabetic, insulin-treated diabetic, and nondiabetic rodents was excised in toto and measured. Despite a net loss in body weight, the diabetic animals showed a near twofold increase in small intestinal weight. This was characterized by a 148% increase in mucosal mass as well as a 39% increase in intestinal smooth muscle mass (P less than 0.05, respectively). The diabetic intestine was significantly longer and had a greater diameter and surface area. Diabetes significantly increased mucosal mass per unit surface area but produced an insignificant decrease in smooth muscle mass per unit surface area. Insulin treatment of the diabetic animals prevented the increase in total mucosal mass and mucosal mass per unit surface area. Insulin treatment also prevented the increase in smooth muscle mass, but reduced smooth muscle mass per unit surface area to a level significantly less than that found in nondiabetic intestine. In vitro dose-response studies of circular and longitudinal small intestinal muscle from the diabetic animals showed normal tension development and sensitivity to both bethanechol chloride and physostigmine. These observations show that the diabetic state produces alterations in not only mucosal but also smooth muscle mass in the small intestine. However, despite these morphological changes, diabetic intestinal smooth muscle retains its sensitivity to cholinergic stimulation and its capacity for tension generation.
Representative longitudinal muscle strips (6 x 10 mm) from distal small intestine were obtained from rats after 1, 2, and 3 mo of streptozocin-induced diabetes. The strips were stretched to their optimum lengths and subjected to electrical field stimulation (1-ms pulse duration, 30-270 mA, 10 Hz) in the presence of Krebs solution and Krebs solution plus 10(-6) M atropine. Field stimulation produced atropine-sensitive and atropine-resistant contractions in all strips. After 1 mo, significant differences in the amplitudes of the atropine-sensitive contractions were found between the diabetic rats and nondiabetic controls. Insulin-treated diabetic rats showed contraction responses that were intermediate in amplitude. After 2 mo, the difference between the control and diabetic groups was less evident but still significant. After 3 mo, the previously noted difference in the atropine-sensitive contractions between the diabetic and control groups had resolved. No significant differences among the three groups were noted in the amplitudes of the atropine-resistant contractions. Field stimulation delivered at pulse durations of 50 ms in the presence of neural blockade with tetrodotoxin (5 x 10(-6) M) produced similar contraction amplitudes among the three groups at any respective time phase of the study. Dose-response studies of intestinal muscle after 3 mo of untreated diabetes showed normal tension development to both bethanechol chloride and physostigmine. These results indicate that streptozocin-induced diabetes is acutely associated with defective cholinergic neuromuscular transmission in the myenteric plexus of the distal small intestine. The abnormality is less evident after 2 mo of untreated diabetes and resolves spontaneously after 3 mo. Insulin treatment appears to accelerate this resolution.
Proximal and distal rat small intestine from 4-, 5- and 6-month-old rats were cut into strips measuring 6.0 X 10.0 mm. Longitudinal strips were cut along the oral-caudal axis of the intestine while circular strips were cut 90 degrees to that axis. The strips were stretched to their optimum lengths and subjected to electrical field stimulation (0.1-1.0 msec pulse duration, 30-270 mA, 1-26 Hz) in the presence of Krebs' solution and Krebs' solution plus 10(-6) M atropine. Field stimulation produced atropine-sensitive and atropine-resistant contractions in these tissues. Significant differences among the three groups were found in the amplitudes of atropine-sensitive contractions in strips from proximal longitudinal muscle. The 6-month-old animals showed the highest amplitude contractions and the 4-month-old the lowest, whereas the 5-month-old animals showed contractions that were intermediate in amplitude. No significant differences were noted among the atropine-resistant contractions. Field stimulation delivered at pulse durations of 5.0 and 50.0 msec in the presence of neural blockade with tetrodotoxin (5 X 10(-6) M) produced similar contraction amplitudes among the three groups. These results show that tension development produced by field stimulation of the proximal intestine increases significantly with age. The increases appear to be due to age-related differences in cholinergic neuromuscular transmission.
The influence of cholinergic and noncholinergic inhibitory nerves was examined in circular and longitudinal muscle from the duodenum. Rodent proximal small intestine was cut into strips measuring 6.0 x 10.0 mm. Strips cut along the oral-caudal axis were called longitudinal strips, whereas those cut 90 degrees to that axis were called circular strips. The strips were stretched to their optimal lengths and subjected to electrical field stimulation in the presence of various concentrations of atropine, pirenzepine or McN-A-343-11. All three drugs inhibited field-stimulated contraction responses and produced or augmented relaxation responses in both muscle layers. All relaxation responses were abolished by tetrodotoxin, indicating they were due to excitation of inhibitory nerves. For each response examined atropine was significantly more potent than pirenzepine (relative potency ratio, 13.36-95.74). The inhibitory effect of McN-A-343-11 on longitudinal muscle was antagonized by both atropine and pirenzepine, indicating the recruitment of cholinergic inhibitory nerves. Neither atropine nor pirenzepine had any effects on inhibitory responses produced by McN-A-343-11 in circular muscle, indicating the recruitment of noncholinergic inhibitory nerves. McN-A-343-11 also increased spontaneous contraction amplitudes in both muscle layers by a direct (tetrodotoxin-resistant) effect on smooth muscle. This effect was also antagonized by atropine and pirenzepine. Thus, both cholinergic and noncholinergic nerves participate in inhibitory neuromuscular transmission in the small intestine. Circular muscle is dominated by a noncholinergic inhibitory innervation. Longitudinal muscle appears to be controlled by both cholinergic and noncholinergic inhibitory nerves.
Explore the source record for details and available documents.