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Biomedical subjects

P Bender

Publications and source records attributed to P Bender.

At least 19 recordsLinked to original sources
PubMed2004

Assessment of right ventricular function by 16-detector-row CT: comparison with magnetic resonance imaging.

The purpose of this study was to determine right ventricular (RV) function from 16-detector-row CT by using two different software tools in comparison with MRI. Nineteen patients underwent cardiac CT. (1) With semiautomated contour detection software end-diastolic and end-systolic RV volumes were determined from short-axis CT reformations (MPR) created at every 10% of the RR-interval. (2) End-systolic and end-diastolic axial images were transformed to 3D to determine the volumes by using a threshold-supported reconstruction algorithm. Steady-state free-precession cine-MRI of the heart was done in short-axis orientation. RV function could not be analyzed in one patient because of sternal wire artifacts in MRI. Mean end-diastolic (155.4+/-54.6 ml) and end-systolic (79.1+/-37.0 ml) RV volumes determined with MPR correlated well with MRI [151.9+/-53.7 ml (r=0.98) and 75.0+/-36.0 ml (r=0.96), respectively (P<0.001)]. RV stroke volume (76.2+/-20.2 ml for MPR-CT, 76.9+/-20.7 ml for MRI, r=0.93) showed a good correlation and RV ejection fraction (50.8+/-8.4% for MPR-CT, 51.9+/-7.4% for MRI, r=0.74) only a moderate one. Threshold supported 3D reconstructions revealed insufficient correlations with MRI (r=0.31-0.59). MPR-based semiautomated analysis of cardiac 16 detector-row CT allows for RV functional analysis. The results correlate well with MRI findings. Threshold value-supported 3D reconstructions did not show satisfying results because of inhomogeneities of RV contrast enhancement.

Aged↗
PubMed2004

[Assessment of global and regional left ventricular function with a 16-slice spiral-CT using two different software tools for quantitative functional analysis and qualitative evaluation of wall motion changes in comparison with magnetic resonance imaging].

PURPOSE: To determine global and regional left ventricular (LV) function from retrospectively gated multidetector row computed tomography (CT) by using two different semiautomated analysis tools and to correlate the results with those of magnetic resonance imaging (MRI). MATERIALS AND METHODS: Nineteen patients (5 females, 14 males, mean age 69 years) underwent 16-slice spiral-CT (MS-CT) with standard technique without administration of beta-blockers for a decrease in the cardiac rate. Ten series of images were reconstructed at every 10 % of the RR-interval. With commercially available software capable of semiautomated contour detection, end-diastolic and end-systolic LV volumes (EDV and ESV) were determined from short-axis multiplanar CT reformations (MPR). Axial images of the end-systolic and end-diastolic cardiac phase were transformed to 3D volumes (3D) to determine EDV and ESV by using a threshold-supported reconstruction algorithm dependent on the contrast enhancement of the left ventricle. Steady-state free-precession cine MR images were acquired in short-axis orientation on the same day in all but one patient. Regional wall motion was assessed qualitatively in 17 left ventricular segments and classified as normo-, hypo-, a- or dyskinetic. Bland-Altman analysis was performed to calculate limits of agreement and systematic errors between CT and MRI. RESULTS: For MPR/3D, mean end-diastolic (144.4/142.8 mL +/- 67.5/67.1) and end-systolic (66.4/68.7 mL +/- 52.1/49.9) LV volumes as determined with MS-CT correlated well with MRI measurements (147.6 mL +/- 67.6 [ r = 0.98/0.96] and 73.3 mL +/- 55.5 [ r = 0.98/0.98], respectively [ p <.001]). LV stroke volume (77.6/74.1 +/- 19.2/23.4 mL for CT vs. 74.4 mL +/- 18.4 for MRI, r = 0.92/0.74) and LV ejection fraction (58.6/55.9 % +/- 13.5/13.7 for CT vs. 55.6 % +/- 13.5 for MRI, r = 0.95/0.91) also showed good correlation (p <.001). Regional wall motion analysis revealed agreement between CT and MRI in 316/323 (97.8 %) myocardial segments. CONCLUSION: Semiautomated analysis of 16-detector row CT data sets enables global and regional volumetric and functional analysis. The CT results correlate well with MRI findings for short axis MPR and for 3D volume reconstructions, with a higher statistical spread for the 3D method. The underestimation of end-systolic and end-diastolic volumes with CT may be caused by partial volume averaging due to the lower temporal resolution as compared with MRI.

Aged↗
PubMed1999

Alcohol-influenced recreational boat operation in the United States, 1994.

BACKGROUND: There were 783 recreational boating fatalities in the United States in 1994. One contributor to this toll is alcohol-influenced operation of boats. Our study objective was to determine the prevalence of alcohol-influenced motor boat operation, and describe its relationship to demographic factors and other risk behaviors. METHODS: In 1994, a randomly dialed national telephone survey contacted 5238 adult respondents who reported on their operation of motor boats, alcohol use, and other potential injury risk behaviors. Data were weighted to obtain national estimates and percentages. RESULTS: Of 597 respondents who operated a motor boat in 1994, 31% (206 respondents) reported doing so at least once while alcohol-influenced. Alcohol-influenced operation of a motor boat was significantly more likely among males, individuals between 25 and 34 years of age, and those with greater than a college education. Alcohol-influenced motor boat operation was also more common among those who drove motor vehicles while alcohol-influenced, and those who drove a motor vehicle without using a seat belt. CONCLUSIONS: To decrease alcohol-influenced boating, new strategies should be developed. Strategies used to decrease drinking and driving motor vehicles may prove adaptable to preventing alcohol-influenced boating. More effective means of monitoring alcohol-influenced boating is needed. Alcohol use by passengers on boats should not be overlooked as a problem.

Accidents↗
PubMed1998

Evaluation of a bicycle helmet giveaway program--Texas, 1995.

OBJECTIVE: To determine the effect of a bicycle helmet giveaway program on helmet use among children. METHODS: In 1995, a bicycle helmet giveaway program was conducted in two rural towns in Texas. Helmets were given to all 403 school children in kindergarten through grade 8. Helmet education, a bicycle rodeo, and incentives to increase helmet use were part of the program. Observations of helmet use were made before the helmet program began and after the program at several intervals throughout the school year and during the summer. A self-reported survey questionnaire was administered to children in grades 4 through 8 before the helmet program began and at several intervals during the school year to determine their attitudes about helmet use, safety perceptions, and peer pressure. A questionnaire also was administered to the parents of these children to determine attitudes and bicycle helmet use among parents. RESULTS: Helmet use increased from 3% before the giveaway to 38% at the end of the school year, 7 months later. However, during the subsequent summer, helmet use decreased to 5%. Helmet use among 7th- and 8th-grade students was 0% at all observations periods after the giveaway. Even though 96% of all students thought that helmet use increased riding safety and 68% thought helmets should be worn at all times when riding, only 25% thought that their friends would approve of helmet use. Most parents also believed that helmets increased riding safety and should be worn, but only 23% reported always wearing one when riding a bicycle. CONCLUSIONS: Bicycle helmet giveaway programs can increase helmet use temporarily, but they may not be sufficient to sustain it. This program was not effective among 7th- and 8th-grade students.

Adolescent↗
PubMed1996

Modification of the cytoplasmic domain affects the subcellular localization of Golgi glycosyl-transferases.

Our goal was to engineer a Golgi glycosyltransferase epitope-tagged on its cytoplasmically exposed, short, N-terminal domain that gave normal subcellular localization. Partial replacement of the cytoplasmic tail of human alpha-2,6-sialyltransferase (SialylT) with the negatively charged myc or FLAG epitope resulted in almost complete mislocalization of the chimera expressed in Vero cells. A granular cytoplasmic staining pattern was seen by immunofluorescence. Spacing the negatively charged residues progressively outward from the negative N-terminus resulted in increasingly more normal localization of myc or FLAG-tagged protein to a juxtanuclear Golgi-like distribution. Substitution of a neutrally charged VSV-G sequence for these tags resulted in normal localization of the chimera to the juxtanuclear Golgi region. Insertion of the myc epitope within the N-terminal domain of the short form of bovine beta-1,4-galactosyltransferase (GalT) gave a chimeric protein that mislocalized in BHK cells. No signal was detected with a monoclonal anti-epitope antibody indicating that the myc epitope was masked. Placement of myc or FLAG epitopes at the NH2-terminus of human N-acetylglucosaminyltransferase I (GlcNAc-T) resulted in chimeric proteins that in Vero cells displayed little Golgi localization. We conclude that positioning of negative charge, in particular, close to the membrane, typically produces a failure of type II Golgi glycosyltransferases to exit the ER/CGN, presumably due to quality control mechanisms. These proteins may be successfully epitope-tagged on their N-terminal domain either using a neutral or positively charged sequence or spacing any negatively charged sequence out from the membrane.

Amino Acid Sequence↗
PubMed1996

Factors associated with nursing interventions to reduce incontinence in hospitalized older adults.

INTRODUCTION: The problem of incontinence in hospitalized elderly patients is rarely documented, and there is little research that determines why nurses choose to help or not help with this problem. Are hospital-based acute care nurses' attitudes and beliefs about incontinence associated with the perceived opportunity to assist the patient with the problem? What do hospital nurses know about causes and interventions relative to incontinence? METHODS: Two vignettes, one describing a patient with stress incontinence and one describing a patient with urge incontinence, were created. Questions measuring variables of a help-giving model were developed, and nurses were asked to mark on a Likert-type scale when answering each question. RESULTS: One hundred-fifty respondents returned completed questionnaires along with three nurse experts. Many hospital nurses believed incontinence was temporary and part of being old. As a group they had a more positive attitude toward intervening for urge incontinence and believed the physician and their nurse manager expected them to assist the patient with urge incontinence. Respondents tended to believe the patient was least likely to expect help. Respondents were evenly divided about opportunity to provide assistance for stress or urge incontinence. Less than half of the nurses correctly listed causes and interventions for stress or urge incontinence. CONCLUSIONS: Other clinical problems perceived as more pressing and lack of knowledge concerning appropriate helping measures affect nurses' perceptions of opportunity to intervene when elderly hospital patients are incontinent. Assessment and intervention are essential to quality nursing care. Undergraduate nursing education and ongoing staff education about incontinence are crucial if assessments and interventions are to be correct. Patients, as health care consumers, have to be more educated about incontinence and choose to have the problem addressed during hospitalization. The Agency for Health Care Policy and Research Clinical Practice Guidelines is a major recommended reference.

Aged↗
PubMed1990

Further studies on growth factor production by the TC-1 stromal cell line: pre-B stimulating activity.

Adherent murine stromal cells support long-term in vitro lymphopoiesis or myelopoiesis dependent on the culture conditions used. A cell line, TC-1, isolated from long-term liquid murine marrow cultures under conditions approaching those permissive for lymphoid growth, has been found to produce an activity that acts synergistically with interleukin-3 (IL-3) or colony-stimulating factor-1 (CSF-1) to stimulate in vitro myeloid colonies, but which has no intrinsic colony-stimulating activity. We report here the presence of multiple growth factors in conditioned medium (CM) from the TC-1 line, including granulocyte-macrophage colony-stimulating factor (GM-CSF) (bioassay with antibody blocking and messenger RNA [mRNA] analysis), granulocyte CSF (G-CSF) and IL-4 (factor-dependent cell line bioassay), and CSF-1 (radioimmunoassay, mRNA) along with a pre-B cell inducing activity, which appears separate from these CSFs and segregates with the myeloid synergizing activity through anion exchange, sizing, and Conconavalin A chromatography. Because these activities are not yet purified to homogeneity, their identity or lack of identity remains an open question. Assays of TC-1 CM or cellular mRNA analysis have given negative results for IL-1, IL-2, IL-3, IL-6, and IL-7, and IL-6 does not stimulate pre-B cells in this assay. However, IL-4 and G-CSF do stimulate in vitro induction of pre-B cells from pre-B and B-cell-depleted Balb/C marrow and are present in CM by selective cell line assay. A monoclonal antibody to IL-4 that inhibited its pre-B inducing activity did not inhibit pre-B inducing activity of TC-1 CM. These data suggest the existence of a unique synergizing and pre-B inducing factor(s) in TC-1 CM. Given the known capacity of subliminal levels of growth factors to act synergistically, an alternate possibility is that these biologic phenomena represent the actions of low concentrations of growth factors acting synergistically and possibly associated with some core protein.

Animals↗
PubMed1990

Pharmacological profile of SK&F 105809, a dual inhibitor of arachidonic acid metabolism.

The effects of SK&F 105809, 6,7,-dihydro-2-[4(methylsulfinyl) phenyl]-3-(4-pyridyl) -5[H]-pyrrolo[1,2-a] imidazole, on eicosanoid metabolism, inflammatory responses, algesia and ulcer formation are described. SK&F 105809 was determined to be a prodrug for the sulfide metabolite SK&F 105561 which is an inhibitor of 5-lipoxygenase (5-LO) and prostaglandin H (PGH) synthase activities seen with both the isolated enzyme (IC50S 3 microM) and human monocyte production of the eicosanoids leukotriene B4 (LTB4, IC50 1.0 microM) and prostaglandin E2 (PGE2, IC50 0.1 microM). In-vivo conversion of SK&F 105809 to the active principle SK&F 105561 was observed in both mice and rats. SK&F 105809 inhibited LTB4 and PGE2 production in vivo in inflammatory exudates as well as the production of LTB4 and thromboxane B2 (TxB2) ex vivo in rat blood. SK&F 105809 inhibited oedema and inflammatory-cell infiltration in arachidonic acid-induced inflammation in the mouse ear and rat paw as well as in carrageenan- and monosodium urate crystal-induced peritonitis. SK&F 105809 was also effective in inhibiting mouse collagen-induced arthritis and associated acute-phase reactant protein. At the same time, these acute and chronic models of inflammation were found to be resistant to the action of selective cyclooxygenase inhibitors such as naproxen. In addition, SK&F 105809 possessed analgesic activity in phenylquinone-induced abdominal constriction assay and inhibited indomethacin-induced ulcers.

Administration, Oral↗
PubMed1986

Leukotriene B4 induces formation of inositol phosphates in rat peritoneal polymorphonuclear leukocytes.

Leukotriene B4 (LTB4) induced rapid breakdown of prelabeled inositol phospholipids in rat peritoneal polymorphonuclear leukocytes (PMNs). Formation of [3H]inositol triphosphate ([3H]IP3) was rapid, with a peak of 250-300% of the control level, after 5-15 sec of exposure to LTB4. Accumulation of [3H]inositol bisphosphate was rapid, peaking after 30 sec of treatment. Accumulation of [3H]inositol monophosphate was also rapid in the presence of LiCl. The kinetics of [3H]IP3, [3H]inositol bisphosphate, and [3H]inositol monophosphate accumulation suggest that LTB4 may interact with receptors in PMNs and activate phospholipase C which in turn induces hydrolysis of inositol-phospholipids. The agonist activities of several LTB4 analogs were employed to investigate the structure-activity relationships of LTB4 receptor-mediated activation of phosphatidylinositol hydrolysis. Increases in [3H]IP3 formation were dependent upon the concentration of LTB4 and the agonist analogs. The rank order potency of these analogs was equivalent to that of the pharmacological activity of LTB4 agonists in the PMN chemotaxis assay. Furthermore, the islet activation protein isolated from Bordetella pertussis inhibited LTB4-induced [3H]IP3 formation. The tumor-promoting phorbol myristate acetate also inhibited LTB4-induced [3H]IP3 formation. The LTB4 receptors on a partially purified PMN membrane were characterized. LTB4 binding to the receptors was stereoselective and specific. The binding affinity (Kd) of [3H] LTB4 to the receptors was 1.3 +/- 0.2 nM. The maximum density of binding was 5.5 +/- 1.8 pmol/mg of protein. The rank order potency of binding affinities of several LTB4 analogs was equivalent to that of the induction of IP3 response induced by LTB4 and analogs. These results suggest that LTB4 may interact with receptors in rat PMNs, activate G protein-regulated phospholipase C, and induce [3H]IP3 formation.

Animals↗
PubMed1985

Binding of histamine and histamine analogs to lymphocyte subsets analyzed by flow cytometry.

The binding of histamine, 4-methylhistamine (a histamine type 2 receptor agonist), cimetidine (a histamine type 2 receptor antagonist), and telemethylhistamine (an inactive analog) to human peripheral blood mononuclear cell subsets was investigated by flow cytometry by using conjugates of these ligands coupled to fluorescein-labeled human serum albumin. Our results indicate that binding of fluorescent protein conjugates of histamine and its analogs does not selectively identify a lymphocyte subset(s) that mediates the immunomodulatory effects of histaminergic ligands. Conjugates with both low (2.5 to 2.8:1) and high (28 to 57:1) ligand to protein coupling ratios were used. No binding above background could be detected for the low mole ratio reagents. The high mole ratio reagents were bound by 95 to 99% of all lymphocytes when used at ligand concentrations of 50 microM or greater. At lower ligand concentrations, the number of lymphocytes exceeding a set fluorescence threshold was decreased, but fluorescence distributions remained unimodal at all concentrations used (1 to 500 microM). Monocytes also bound the high mole ratio reagents and gave rise to a second high-intensity peak in the fluorescence distribution unless they were excluded by other means. Levels of conjugate binding detected by flow cytometry did not parallel ligand potencies at classical histamine type 2 receptors; at equivalent ligand concentrations, approximately equal amounts of histamine or 4-methylhistamine conjugate were bound per lymphocyte, and only 30% less telemethylhistamine conjugate was bound. Competition with free ligands (10(2)- to 10(4)-fold excess histamine, 4-methylhistamine, cimetidine, or telemethylhistamine) did not significantly decrease the level of binding observed for the high mole ratio reagents at bound ligand concentrations of 1 to 25 microM. Dual staining with fluorescein-labeled conjugate and phycoerythrin-labeled monoclonal antibodies Leu-3ab (anti-helper T), Leu-2a (anti-suppressor T), Leu-M3 (anti-monocyte), or anti-HLA-DR (B cells and monocytes) was also carried out. The extent of conjugate binding to helper and suppressor cells was identical for each of the ligands used, but higher levels of conjugate binding were seen for monocytes and B cells than for T cells in every case. Our data do not exclude the possibility of enhanced conjugate binding to small numbers of activated (HLA-DR positive) T cells that might be involved in mediation of histamine effects.(ABSTRACT TRUNCATED AT 400 WORDS)

Binding Sites↗
PubMed1984

Differential subcellular localization of tubulin and the microtubule-associated protein MAP2 in brain tissue as revealed by immunocytochemistry with monoclonal hybridoma antibodies.

The distribution and subcellular localization of tubulin and MAP2 in brain tissue were analyzed by immunocytochemistry with monoclonal hybridoma antibodies prepared against Chinese hamster brain tubulin and MAP2. We examined three anti-tubulin hybridoma antibodies (Tu3B, Tu9B, Tu12) specific for beta-tubulin, and two anti-MAP2 hybridoma antibodies (AP9,AP13). The specificity of each of the monoclonal antibodies was characterized by staining nitrocellulose electrophoretic blots of SDS-polyacrylamide gels of whole brain or hippocampal extracts. Each hybridoma antibody bound only its respective antigen in these preparations. Polyclonal antisera against tubulin were also examined. Sections reacted with antisera against tubulin or monoclonal antibodies against beta-tubulin revealed a wide variety of stained cellular compartments. The reaction product was found to decorate dendritic and axonal microtubles in neurons; glial cells were also stained. MAP2 immunoreactivity was found only in neurons. In the case of one of the monoclonal antibodies (AP9), staining was preferentially associated with dendritic processes. However, light but significant staining of axonal processes was seen with AP13. Within dendrites, MAP2 was found associated with dendritic microtubules and postsynaptic densities (psd), both in shaft and spine synapses. In addition, strong immunoreactivity for MAP2 was found within the cytoplasm of dendritic spines. There was little or no immunoreactivity for tubulin in the spine cytoplasm, although the psd was stained. The localization of MAP2 in dendritic spines and in the psd suggests that this protein may have a biological role independent of its association with microtubules. The observations on differential staining of the hybridoma antibodies against MAP2 suggest that there may be distinct subtypes or states of MAP2 within neurons.

Animals↗
PubMed1983

Distribution and subcellular localization of calmodulin in adult and developing brain tissue.

The distribution and subcellular localization of calmodulin in adult and developing cerebellum was studied in rats by immunocytochemistry. Calmodulin immunoreactivity was found both in neurons and in glial cells. Within neurons the staining was particularly intense in the cell nucleus and in dendrites, the cytoplasm of the cell body was more lightly stained than the nucleus, and light immunoreactivity was observed in axons. Electron microscopic analysis confirmed the association of calmodulin with the nuclear chromatin, while the nucleolus remained unstained. The reaction product was also found overlying the membranes of several organelles, in postsynaptic densities and decorating both dendritic and axonal microtubules. In developing Purkinje cells, calmodulin immunoreactivity was found as early as 5 days after birth. During the initial phases of dendritic development (5-10 days post-natal), the reaction product was associated with the organelles of the apical cone, while little or no staining was observed in the elongating dendrites or in the cell nucleus. Later in development, calmodulin was found in primary and secondary dendrites, and by 20 days after birth immunoreactivity appeared in the cell nucleus, and in the postsynaptic densities of immature spines located in dendrites. The presence of calmodulin in the apical cone suggests the possibility that this protein may participate in the regulation of microtubule formation during the initial stages of dendritic development. Its presence in dendrites at later stages (during the period of synaptogenesis) may indicate that it also participates in the formation of synapses between the parallel fibres and dendritic spines.

Animals↗