Identification of the first vancomycin-resistant Enterococcus faecalis harbouring vanE in Canada.
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Amoxicillin↗
Biomedical subjects
D Boyd
Publications and source records attributed to D Boyd.
Heregulin regulation of urokinase plasminogen activator and its receptor: human breast epithelial cell invasion.
Heregulin-beta1, which binds human epidermal growth factor receptors 3 and 4, promotes motility and invasiveness of breast cancer cells. Considering the established role of urokinase plasminogen activator (uPA) and its receptor (uPAR) in invasion, this study was undertaken to explore the role of heregulin-beta1 in regulating uPA and uPAR in breast cancer invasion. The stimulation by heregulin-beta1 of noninvasive human breast cancer MCF-7 cells induced the expression of uPA mRNA, protein, and its plasminogenic activity. This uPA mRNA expression was blocked by a transcriptional inhibitor, actinomycin D, and does require de novo protein synthesis for its optimal induction in MCF-7 cells, but not in mouse mammary epithelial HC11 cells. Heregulin-beta1 also induced the expression of uPAR mRNA and protein in an actinomycin D-sensitive manner and cycloheximide superinduced the uPAR mRNA. Heregulin-beta1-stimulated signaling initiated the transcription from uPA- and uPAR-promoters. These results suggest that heregulin-beta1 regulation of breast cancer cell invasion may be mediated in part through the up-regulation of uPA and uPAR.
Breast Neoplasms↗
Adapting the HCUP QIs for hospital use: the experience in New York State.
BACKGROUND: The Agency for Healthcare Research and Quality developed the Healthcare Cost and Utilization Project (HCUP) quality indicators (QIs) in 1994. The Healthcare Association of New York State (HANYS; Albany), which represents more than 500 nonprofit and public hospitals, long-term care facilities, and home health care agencies, has adapted the HCUP QIs since 1997 to produce annual comparative reports for its member hospitals. Specifically designed for internal use, the reports have been well received and have drawn interest from other hospital associations and state health departments. METHODS: The HCUP QIs were applied to the New York State hospital discharge abstract. A risk adjustment model was constructed for each complication measure. Measures of utilization and access to care were adjusted for differences in patient demographics and payer status by indirect standardization. Data are presented in graphic format. Each hospital receives its own report (in both paper copy and CD-ROM) with comparisons to statewide norms, regional averages, and peer group averages. Report prepared for hospital systems include data for each affiliated hospital. CONCLUSIONS: When used appropriately, the HCUP QIs provide valuable information for individual hospitals to assess quality of care and target potential areas for improvement. The HCUP QIs also give hospitals a broad perspective to look beyond their own institutions and develop community-based quality improvement initiatives. Nevertheless, given the limitations that commonly exist with administrative databases and the lack of standard risk adjustment systems, the HCUP QIs are best used for internal purposes and not for public reporting.
Benchmarking↗
Ectopic parotid gland as an unusual cause of cheek swelling.
There are numerous causes for chronic cheek swelling, including masseteric hypertrophy, lymphadenopathy, diffuse inflammatory changes and neoplasia. We report an unusual case where the swelling was the result of ectopic parotid tissue.
Adult↗
Improved primer design for multiplex PCR analysis of vancomycin-resistant Enterococcus spp.
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Animals↗
Regulation of the uPA gene in various grades of human glioma cells.
Urokinase-type plasminogen (uPA) activator regulates a variety of processes, including morphogenesis, cell differentiation, migration, and invasion. In previous studies, we demonstrated that uPA levels are significantly higher in anaplastic astrocytoma and glioblastoma than in low-grade glioma and normal brain tissue. In the present study, our goal was to determine whether the increase in uPA production in higher-grade gliomas is caused by an increase in mRNA stability or increased transcription of the gene in three human glioma cell lines of various grades (H4, SW1783, UWR3). The half-life of uPA mRNA was about 14 h in UWR3 and 8 h in SW1783 cells. In transient transfection studies of the wild-type -2109-bp human uPA promoter in the different grades of cell lines, the uPA promoter activity was increased two-fold in SW1783, anaplastic astrocytoma cells and six-fold in UWR3 glioblastoma cells, as compared with the uPA promoter activity in low-grade H4 cells. Using human uPA promoter chloramphenicol acetyl transferase (CAT) constructs with mutations of the AP-1 element at -1967 or the PEA-3 cis element at -1973, the activity of the uPA promoter was decreased 4-fold to 10-fold in all three human glioma cell lines. In transient transfection assays, the uPA promoter was stimulated 2.2-fold in UWR3 and SW1783 cells and 3.7-fold in H4 cells in response to phorbol-12-myristat-13-acetate. We further studied the activation and inhibition of uPA promoter by co-expression of a transactivation domain lacking c-jun: a dominant negative ERK1 and ERK2 mutant and a dominant negative c-raf in glioblastoma cell line showed repressed uPA promoter activity compared with the effect of the empty expression vector. We conclude from our findings that increased transcription is the more likely mechanism underlying the increase in uPA production in high-grade gliomas.
Gene Deletion↗
Regulation of the urokinase-type plasminogen activator receptor gene in different grades of human glioma cell lines.
We reported previously that the production of urokinase-type plasminogen activator receptor (uPAR) protein is greater in high-grade glioblastomas than in low-grade gliomas. Transcriptional activation of the uPAR gene or increased stability of the uPAR mRNA that encodes this protein could cause the increased production of this protein in cell lines of different grades of gliomas. We found similar half-life of uPAR mRNA of 10-12 h in glioblastoma multiforme (UWR3) and anaplastic astrocytoma (SW1783) cells. However, the human uPAR promoter was up-regulated 6-8-fold in SW1783 cells and 11-13-fold in UWR3 cells as compared with its activity in low-grade gliomas, a finding that correlates well with previous findings of increases in uPAR mRNA and protein levels in higher-grade gliomas. uPAR mRNA level was increased 11-fold over a 24-h period in low-grade glioma cell lines after treatment with phorbol myristate acetate. The region spanning -144 to -123 bp of the human uPAR promoter that contains the Sp-1 site and a PEA-3 element and an AP-1 site at -184 plays major roles in uPAR promoter activity in glioblastoma cells. Specific antibodies used in an electrophoretic mobility shift assay identified fra-1, fra-2, Jun D, and c-Jun proteins in the nuclear protein complex that bind a 51-mer containing the AP-1 consensus sequence at -184 and its flanking sequences in the uPAR promoter. We further studied the inhibition of uPAR promoter by coexpression of a transactivation domain lacking C-Jun; a dominant-negative ERK1 and ERK2 mutant and a dominant-negative C-raf in glioblastoma cell lines showed the repressed uPAR promoter activity compared with the effect of the empty expression vector. We conclude from our findings that increased transcription is the more likely mechanism underlying the increase in uPAR production in high-grade gliomas.
Chloramphenicol O-Acetyltransferase↗
A mutant hunt for defects in membrane protein assembly yields mutations affecting the bacterial signal recognition particle and Sec machinery.
We describe an Escherichia coli genetic screen that yields mutations affecting two different cellular processes: disulfide bond formation and membrane protein assembly. The mutants defective in disulfide bond formation include additional classes of dsbA and dsbB mutations. The membrane protein assembly defective mutants contain a mutation in the secA operon and three mutations in the ffs gene, which encodes 4.5S RNA. These latter mutations are the only ones to be isolated in a gene encoding a component of the bacterial signal recognition particle by screening in vivo for defects in membrane protein insertion. A sensitive method for examining membrane protein localization shows that the ffs and secA locus mutations affect membrane assembly of the polytopic membrane protein, MalF. The ffs mutations also affect the membrane insertion of the FtsQ and the AcrB proteins. Although both the ffs and the secA locus mutations interfere with membrane protein assembly, only the latter also reduces export of a protein containing a cleavable signal sequence.
Adenosine Triphosphatases↗
Coccidioidomycosis in human immunodeficiency virus-infected persons in Arizona, 1994-1997: incidence, risk factors, and prevention.
From 1 January 1995 through 31 June 1997, 153 cases of coccidioidomycosis in human immunodeficiency virus (HIV)-infected persons were identified in Arizona (incidence, 41/1000 persons living with AIDS). A case-control study was conducted to evaluate risk factors for coccidioidomycosis in HIV-infected persons. A case was defined as laboratory-confirmed, incident coccidioidomycosis in a person infected with HIV for > or =3 months, and each case patient had 3 control patients matched by county, age group, sex, HIV/AIDS status, and CD4 lymphocyte count. Multivariable analysis identified black race and a history of oropharyngeal or esophageal candidiasis to be associated with increased risk of coccidioidomycosis; protease inhibitor therapy was associated with a reduced risk. In persons with previous history of oropharyngeal or esophageal candidiasis, having received an azole drug was associated with a reduced risk (odds ratio, 0.4; 95% confidence interval, 0.2-0.9; P=.04). Physicians may need to consider azole chemoprophylaxis for HIV-infected persons who live in areas of endemicity, have CD4 cell counts <200/microL, are black, or have a history of thrush.
AIDS-Related Opportunistic Infections↗
9:45-10:00. Superimposition of EBCT Determined Coronary Calcium Deposits onto Myocardial PET Perfusion Images by Rubidium-82 and Nitrogen-13 Ammonia for Assessment of Flow Limiting Defects.
Calcium localization by Electron Beam CT (EBCT) in the coronary arteries is becoming an important non-invasive method for screening asymptomatic patients for early coronary atherosclerosis. However, the relationship between coronary artery calcium deposits and myocardial perfusion abnormalities has not been established. We have developed software to superimpose location of coronary calcium by EBCT onto PET myocardial perfusion images, so that we can determine the role of location and amount of calcium in the arteries to flow-limiting perfusion defects by PET.EBCT and PET transaxial images are each first converted to three-dimensional arrays of 1 mm voxels. The resulting two image volumes sets are displayed so that a vertical line can be drawn from the clavicle to the spine for proper rotation of the body. The rotated images are then displayed superimposed and are shifted in the vertical, horizontal, and the long axis directions to co-register the EBCT and PET images. The EBCT images are windowed for calcium Houndsfield numbers and calcium location is added to the PET images as a maximum intensity value in the image. The modified PET image volume is then translated back to the PET data format and reprocessed using cardiac analysis software such that the calcium location is superimposed on the PET myocardial perfusion images.Preliminary results of the PET-EBCT superimposition program correlate with location of coronary calcium by EBCT and PET perfusion defects following stress. This technique may be useful for identifying flow-limiting calcium deposits in the coronary arteries.
Journal Article↗
Individualized mouth prop for dental professionals and carers.
Maintaining a high standard of dental health in children with special needs, particularly those who are unable to control mandibular activity, can prove difficult and time consuming for parents, carers and dental professionals. This article describes the construction of an individually made and relatively unobtrusive finger guard mouth prop, designed to facilitate intraoral examination and oral hygiene care for these children. An initial evaluation by a number of users found these mouth props were simple to fit, stable and provided adequate finger protection. All users planned to continue using their mouth prop after the trial period. It is concluded that similar finger mounted mouth props may help facilitate dental care and oral hygiene for children requiring special care.
Bites, Human↗
Identification of a novel nuclear factor-kappaB sequence involved in expression of urokinase-type plasminogen activator receptor.
We have previously defined the promoter of human urokinase-type plasminogen activator receptor (uPAR) gene in a 188-bp fragment between bases -141 and +47 relative to the translation start site. Here, we report that a novel nuclear factor-kappaB (NF-kappaB)-like sequence (5'-GGGAGGAGTC-3') at -45 is located in the uPAR promoter and one of the two DNase I-protected regions, region I between bases -51 and -30. This NF-kappaB-like motif differs at positions 7-9 from the decameric consensus sequences of NF-kappaB (5'-GGGRNNYYCC-3' where R indicates A or G, Y indicates C or T, and N indicates any nucleotide) and at positions 1 and 7-9 from the kappaB-like motifs (5'-HGGARNYYCC-3' where H indicates A, C, or T, R indicates A or G, Y indicates C or T, and N indicates any nucleotide). Nuclear extracts from HCT116 cells contain proteins that specifically bind to the NF-kappaB-like site at position -45. Mutation of the NF-kappaB-like motif decreased the binding of transcription factor NF-kappaB and reduced the uPAR promoter activity in comparison with the wild-type sequences. Co-transfection with a dominant negative I-kappaB kinase-2 expression vector reduced uPAR promoter activity by 65-75%. These results demonstrate that a previously uncharacterized NF-kappaB motif is required for uPAR promoter activity.
5' Untranslated Regions↗
Effect of subarachnoid morphine administration on extubation time after coronary artery bypass graft surgery.
OBJECTIVE: To determine the effects of 2 low doses of intrathecal morphine on extubation time and on postoperative analgesic requirements after coronary artery bypass graft (CABG) surgery. DESIGN: A prospective, randomized, double-blind, placebo-controlled study. SETTING: Tertiary-care university hospital. PARTICIPANTS: Fifty adult patients scheduled for elective primary CABG surgery. INTERVENTIONS: Patients were randomized to receive placebo, 250 microg, or 500 microg intrathecal morphine, preoperatively. Intraoperative fentanyl and midazolam were limited to 15 microg/kg and 20 microg/kg intravenously. Patients were extubated in the intensive care unit by a blinded observer using predefined extubation criteria. MEASUREMENTS AND MAIN RESULTS: Time to extubation and postoperative requirements for morphine, midazolam, nitroglycerin, and sodium nitroprusside were recorded by a blinded observer. Extubation times were 441 +/- 207 minutes versus 325 +/- 188 minutes versus 409 +/- 245 minutes for the placebo, 250-microg, and 500-microg groups (p = 0.27). Postoperative morphine requirements in the 250-microg and 500-microg groups were 13.6 +/- 7.8 mg and 11.7 +/- 7.4 mg, compared with 21.3 +/- 6.2 mg in the placebo group (p = 0.001). There were no differences among the study groups with regard to postoperative midazolam, nitroglycerin, and sodium nitroprusside requirements. CONCLUSIONS: Despite decreased postoperative morphine requirements, intrathecal morphine administration did not have a clinically relevant effect on extubation time after CABG surgery. This study suggests that 250 microg is the optimal dose of intrathecal morphine to provide significant postoperative analgesia without delaying tracheal extubation.
Adolescent↗
The ArcB sensor kinase of Escherichia coli: genetic exploration of the transmembrane region.
The Arc two-component signal transduction system of Escherichia coli regulates the expression of numerous operons in response to respiratory growth conditions. Cellular redox state or proton motive force (Delta(H(+))) has been proposed to be the signal for the membrane-associated ArcB sensor kinase. This study provided evidence for a short ArcB periplasmic bridge that contains a His47. The dispensability of this amino acid, the only amino acid with a pK in the physiological range, renders the Delta(H(+)) model unlikely. Furthermore, results from substituting membrane segments of ArcB with counterparts of MalF indicate that the region does not play a stereospecific role in signal reception.
Alkaline Phosphatase↗
Towards single-copy gene expression systems making gene cloning physiologically relevant: lambda InCh, a simple Escherichia coli plasmid-chromosome shuttle system.
We describe a simple system for reversible, stable integration of plasmid-borne genes into the Escherichia coli chromosome. Most ordinary E. coli strains and a variety of pBR322-derived ampicillin-resistant plasmids can be used. A single genetic element, a lambda phage, is the only specialized vector required. The resultant strains have a single copy of the plasmid fragment inserted stably at the lambda attachment site on the chromosome, with nearly the entire lambda genome deleted.
Ampicillin Resistance↗
20 of the most influential people in EMS. Part 2. Interview by Mike Taigman.
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Emergency Medical Services↗
Candida albicans: adherence, signaling and virulence.
The focus of this symposium was to present new information on the morphogenesis of Candida albicans, particularly how it relates to signal transduction pathways and other genes involved in the regulation of morphogenesis. In addition, we discuss the role of adherence and colonization of the oral cavity by the organism and discuss the role of mannan as an adhesin that recognizes the human red blood cell. C. albicans utilizes at least two signal pathways to regulate its conversion from a yeast form to filamentous growth (hyphae). One of these two pathways is similar to the Saccharomyces cerevisiae pseudohyphal/mating pathway, which utilizes the regulatory protein, Cphlp. The other pathway is not totally defined but requires a second regulatory protein, referred to as Efg1p. Other signal pathways may exist, which include a two-component histidine kinase and response regulator proteins. The latter pathway(s) may include proteins such as Chk1p, Ssk1p, Shi1p and Cos1p/Nik1p. Mutations in strains, which specifically target these proteins, result in morphogenesis defects and avirulence or attenuation of strains. A growth regulatory gene has also been recently defined whose expression is associated with growth cessation and which appears to be a necessary prerequisite in conversion of the organism to a filamentous growth form. Starvation of yeast cells induces exponentially grown cells (and usually non-germinative) to germinate. This phenomenon is also observed in cells that are transiently treated with metabolic inhibitors. During each of these treatments (starvation, metabolic inhibition), expression of a growth regulatory gene (CGRI) increases. Adherence of C. albicans to host cells and tissues is complex; several proteins, which appear to have host recognition functions, have been defined. In the oral cavity, C. albicans selectively adheres to salivary proteins, which are absorbed to many oral surfaces. This mechanism enables the cells to colonize surfaces of the oral cavity. An understanding of these interactions may lead to strategies to prevent oral disease. Mannan from C. albicans may provide a host recognition function for C. albicans. Recent experiments indicate that mannan binds to human red blood cells and causes hemolysis. Binding of mannan to the band 3 protein of human red blood cells has been established. This activity may be associated with the ability of the organism to utilize hemoglobin (and iron).
Candida albicans↗
Regulation of BAD phosphorylation at serine 112 by the Ras-mitogen-activated protein kinase pathway.
The function of the pro-apoptotic molecule BAD is regulated by phosphorylation of two sites, serine-112 (Ser-112) and serine-136 (Ser-136). Phosphorylation at either site results in loss of the ability of BAD to heterodimerize with the survival proteins BCL-XL or BCL-2. Phosphorylated BAD binds to 14-3-3 and is sequestered in the cytoplasm. It has been shown that phosphorylation of BAD at Ser-136 is mediated by the serine/threonine protein kinase Akt-1/PKB which is downstream of phosphatidylinositol 3-kinase (PI3K). The signaling process leading to phophorylation of BAD at Ser-112 has not been identified. In this study, we show that phosphorylation of the two serine residues of BAD is differentially regulated. While Ser-136 phosphorylation is concordant with activation of Akt, Ser-112 phosphorylation does not correlate with Akt activation. Instead, we demonstrate that activated Ras and Raf, which are upstream of mitogen-activated protein kinases (MAPK), stimulate selective phosphorylation of BAD at Ser-112. Furthermore, phosphorylation of Ser-112, but not Ser-136 requires activation of the MAPK pathway as the MEK inhibitor, PD 98059, blocks EGF-, as well as activated Ras- or Raf-mediated phosphorylation of BAD at Ser-112. Therefore, the PI3K-Akt and Ras-MAPK pathways converge at BAD by mediating phosphorylation of distinct serine residues.
3T3 Cells↗