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Biomedical subjects

J Wiener

Publications and source records attributed to J Wiener.

At least 19 recordsLinked to original sources
PubMed2001

Direct measurement of the pion valence-quark momentum distribution, the pion light-cone wave function squared.

We present the first direct measurements of the pion valence-quark momentum distribution which is related to the square of the pion light-cone wave function. The measurements were carried out using data on diffractive dissociation of 500 GeV/c pi(-) into dijets from a platinum target at Fermilab experiment E791. The results show that the /q&q> light-cone asymptotic wave function describes the data well for Q2 approximately 10 (GeV/c)(2) or more. We also measured the transverse momentum distribution of the diffractive dijets.

Journal Article↗
PubMed2001

Observation of color-transparency in diffractive dissociation of pions.

We have studied the diffractive dissociation into dijets of 500 GeV/c pions scattering coherently from carbon and platinum targets. Extrapolating to asymptotically high energies (where t(min)-->0), we find that when the per-nucleus cross section for this process is parametrized as sigma = sigma0Aalpha, alpha has values near 1.6, the exact result depending on jet transverse momentum. These values are in agreement with those predicted by theoretical calculations of color-transparency.

Journal Article↗
PubMed2001

Search for rare and forbidden Charm Meson decays D0 --> Vl+l- and hhll.

We report results of a search for flavor-changing neutral current (FCNC), lepton flavor, and lepton-number violating decays of the D0 (and its antiparticle) into three and four bodies. Using data from Fermilab charm hadroproduction experiment E791, we examine modes with two leptons (muons or electrons) and a rho(0), K( *0), or straight phi vector meson or a nonresonant pi(pi), Kpi, or KK pair of pseudoscalar mesons. No evidence for any of these decays is found. Therefore, we present branching-fraction upper limits at 90% confidence level for the 27 decay modes examined (18 new).

Journal Article↗
PubMed2001

Study of the D(+)(s)-->pi(-)pi(+)pi(+) decay and measurement of f(0) masses and widths.

From a sample of 848+/-44 D(+)(s)-->pi(-)pi(+)pi(+) decays, we find gamma(D(+)(s)-->pi(-)pi(+)pi(+))/gamma(D(+)(s)-->straight phipi(+)) = 0.245+/-0.028(+0.019)(-0.012). Using a Dalitz plot analysis of this three body decay, we find significant contributions from the channels rho(0)(770)pi(+), rho(0)(1450)pi(+), f(0)(980)pi(+), f(2)(1270)pi(+), and f(0)(1370)pi(+). We also present the values obtained for masses and widths of the resonances f(0)(980) and f(0)(1370).

Journal Article↗
PubMed2001

Experimental evidence for a light and broad scalar resonance in D(+) --> pi(-)pi(+)pi(+) decay.

From a sample of 1172 +/- 61 D(+)-->pi(-)pi(+)pi(+) decays, we find gamma(D(+)-->pi(-)pi(+)pi(+))/gamma(D(+)-->K-pi(+)pi(+)) = 0.0311 +/- 0.0018(+0.0016)(-0.0026). Using a coherent amplitude analysis to fit the Dalitz plot of these decays, we find strong evidence that a scalar resonance of mass 478(+24)(-23) +/- 17 MeV/c(2) and width 324(+42)(-40) +/- 21 MeV/c(2) accounts for approximately half of all decays.

Journal Article↗
PubMed2001

Confidentiality and paradox: the location of ethical space.

Implicit in Jung's alchemical metaphor of the vas bene clausum is the idea of an analytic frame with a space inside it for something vital, a relationship between two selves, to develop. For this to happen, analysts must respect their patients' rights to confidentiality. The paper explores the analyst's state of mind and the intrapsychic processes that are constellated when struggling with ethical dilemmas about issues of confidentiality in analytic work. The author suggests that at times when analysts consider breaking confidentiality, there is often a disturbing inner conflict between their moral principles (codes of ethics) and their internal personal ethical attitude. At these difficult moments, the mutuality of the work and the vas bene clausum can be significantly disrupted. The analyst tries to find a third position, a mental and emotional ethical space where the subjective and the objective, the ethical and the unethical can become more companionable bedfellows.

Confidentiality↗
PubMed2000

A second-stage partogram.

OBJECTIVE: To describe a second-stage partogram based on a system of scoring the descent and position of the fetal head and to use this system for studying progress in the second stage of labor and predicting mode of delivery and obstetric outcome. METHODS: A prospective observational study of 1413 women at term with a singleton, cephalic presentation. The position and station of the fetal head were observed and scored at diagnosis of the second stage of labor, 1 hour later, and then at 30 minute intervals until delivery was achieved. The score at diagnosis of the second stage of labor was assessed for its ability to predict eventual mode of delivery and duration of labor. A normogram was defined for nulliparas and multiparas and was used to define normal and abnormal progress in the second stage, associated factors in the first stage of labor, and mode of delivery. RESULTS: Increasing total score at the start of the second stage of labor is associated with increasing chance of spontaneous vaginal delivery (odds ratio [OR] 1.68 for nulliparas, 1.59 for multiparas), decreasing chance of instrumental vaginal delivery (OR 0.67 for nulliparas, 0.64 for multiparas), and emergency cesarean delivery (OR 0.39 for nulliparas). Abnormal progress as defined by the normogram is associated with use of epidural anesthesia, induction of labor, augmentation, dystocia, and increased incidence of operative delivery. No significant difference is found between normal and abnormal second stages of labor in fetal outcome as determined by Apgar scores. CONCLUSION: The second-stage partogram offers an objective basis for management of the second stage of labor.

Delivery, Obstetric↗
PubMed2000

Anti-HER2 antibody and heregulin suppress growth of HER2-overexpressing human breast cancer cells through different mechanisms.

Previous reports have shown that certain anti-HER2 antibodies and heregulin can inhibit clonogenic growth of breast and ovarian cancers that overexpress HER2. Anti-HER2 antibodies bind to HER2 directly, whereas heregulin does not bind to HER2 alone, but rather interacts with HER2 through the formation of heterodimers with HER3 or HER4. The purpose of the present study was to elucidate the mechanisms by which anti-HER2 antibody and heregulin inhibit tumor growth. The anti-HER2 monoclonal antibody (mAb) ID5 was found to block G1-S progression of the cell cycle, whereas heregulin inhibited passage through G2-M. Compatible with the effects on the cell cycle, treatment with mAb ID5 decreased levels of cyclin-dependent kinase (CDK) 2, cyclin E, and CDK6 proteins and reduced cyclin E-CDK2-associated kinase activity; mAb HD5-treated cells had increased p27Kip1 expression and an increased association of p27Kip1 with CDK2. In contrast, treatment with heregulin increased protein levels of CDK2, CDK6, CDC2, and cyclin B1. More Retinoblastoma protein was found in the hypophosphorylated state in the cells treated with mAb ID5, whereas more retinoblastoma protein was in the hyperphosphorylated state in heregulin-treated cells. Heregulin was able to induce cell differentiation as assessed by Oil Red O staining and apoptosis as assessed by sub-G1 peak on flow cytometry and the presence of DNA fragmentation in ApopTag histochemistry staining. Neither differentiation nor apoptosis was observed in the cells treated with mAb ID5. We conclude that anti-HER-2 mAb ID5 and heregulin exert growth inhibition through different mechanisms. In mammary cells overexpressing HER2, anti-HER2 mAb ID5 induces G1 arrest, whereas heregulin induces G2-M arrest, cell differentiation, and apoptosis.

Androstadienes↗
PubMed1999

Multiple antibiotic-resistant Klebsiella and Escherichia coli in nursing homes.

CONTEXT: Infections caused by ceftazidime sodium-resistant gram-negative bacteria that harbor extended-spectrum beta-lactamases (ESBLs) are increasing in frequency in hospitals in the United States. OBJECTIVES: To report a citywide nursing home-centered outbreak of infections caused by ESBL-producing gram-negative bacilli and to describe the clinical and molecular epidemiology of the outbreak. DESIGN: Hospital-based case-control study and a nursing home point-prevalence survey. Molecular epidemiological techniques were applied to resistant strains. SETTINGS: A 400-bed tertiary care hospital and a community nursing home. PATIENTS: Patients who were infected and/or colonized with ceftazidime-resistant Escherichia coli, Klebsiella pneumoniae, or both and controls who were admitted from nursing homes between November 1990 and July 1992. MAIN OUTCOME MEASURES: Clinical and epidemiological factors associated with colonization or infection by ceftazidime-resistant E coli or K pneumoniae; molecular genetic characteristics of plasmid-mediated ceftazidime resistance. RESULTS: Between November 1990 and October 1992, 55 hospital patients infected or colonized with ceftazidime-resistant E coli, K pneumoniae, or both were identified. Of the 35 admitted from 8 nursing homes, 31 harbored the resistant strain on admission. All strains were resistant to ceftazidime, gentamicin, and tobramycin; 96% were resistant to trimethoprim-sulfamethoxazole and 41% to ciprofloxacin hydrochloride. In a case-control study, 24 nursing home patients colonized with resistant strains on hospital admission were compared with 16 nursing home patients who were not colonized on hospital admission; independent risk factors for colonization included poor functional level, presence of a gastrostomy tube or decubitus ulcers, and prior receipt of ciprofloxacin and/or trimethoprim-sulfamethoxazole. In a nursing home point-prevalence survey, 18 of 39 patients were colonized with ceftazidime-resistant E coli; prior receipt of ciprofloxacin or trimethoprim-sulfamethoxazole and presence of a gastrostomy tube were independent predictors of resistance. Plasmid studies on isolates from 20 hospital and nursing home patients revealed that 17 had a common 54-kilobase plasmid, which conferred ceftazidime resistance via the ESBL TEM-10, and mediated resistance to trimethoprim-sulfamethoxazole, gentamicin, and tobramycin; all 20 isolates harbored this ESBL. Molecular fingerprinting showed 7 different strain types of resistant K pneumoniae and E coli distributed among the nursing homes. CONCLUSIONS: Nursing home patients may be an important reservoir of ESBL-containing multiple antibiotic-resistant E coli and K pneumoniae. Widespread dissemination of a predominant antibiotic resistance plasmid has occurred. Use of broad-spectrum oral antibiotics and probably poor infection control practices may facilitate spread of this plasmid-mediated resistance. Nursing homes should monitor and control antibiotic use and regularly survey antibiotic resistance patterns among pathogens.

Aged↗
PubMed1998

Mitogenic effect of angiotensin II on rat carotid arteries and type II or III mesenteric microvessels but not type I mesenteric microvessels is mediated by endogenous basic fibroblast growth factor.

In this study, anti-basic fibroblast growth factor (anti-bFGF) antibody was used to determine whether the mitogenic effect of angiotensin II in vivo could be blocked by neutralizing bFGF in the vessel wall. Animals, divided into six experimental groups, were given (1) angiotensin II, (2) angiotensin II + anti-bFGF antibody, (3) angiotensin II + normal goat IgG (ngIgG), (4) anti-bFGF antibody, (5) ngIgG, and (6) Ringer's solution. Angiotensin II at 435 ng x kg(-1) x min(-1) was infused into rats continuously for 1 week to induce smooth muscle cell replication, and anti-bFGF antibody or ngIgG was injected intravenously 4 times over the 1-week period at a dose of 60 mg/injection. Bromodeoxyuridine (30 mg/mL) was also continuously infused during the 1-week period. The left carotid artery of all animals was balloon-injured on day 4 of the treatment, and all groups were killed for study on day 7. The results showed that angiotensin II significantly stimulated smooth muscle replication in the balloon-injured carotid artery, intact carotid artery, and three branch levels of the mesenteric vascular tree. Anti-bFGF was able to block the mitogenic effect of angiotensin II in larger vessels but not the smallest (type I) microvessels of the mesenteric arterial tree. This differential response may be attributable to the nature of the lesions in type I vessels versus larger vessels: the type I vascular lesion has a large component of proliferating macrophages, whereas the larger vessels show less injury, few macrophages, and varying levels of smooth muscle replication. Our data suggest that the vessel wall remodeling in the angiotensin II-treated larger vessels involves DNA replication that is dependent on the presence of bFGF.

Angiotensin II↗
PubMed1998

Pure endotoxin does not pass across the intestinal epithelium in vitro.

Numerous reports suggest that endotoxin (LPS) may play a central role in triggering the inflammatory cascade that leads to the systemic inflammatory response syndrome. Although conditions that promote bacterial translocation in vivo may also facilitate direct translocation of LPS, the exact mechanisms by which LPS crosses the intestinal barrier to reach the systemic circulation are unknown. This study was designed to determine whether pure endotoxin could pass across injured rat ileal mucosa in the Ussing chamber. Sprague-Dawley rats were subjected to mild or severe hemorrhagic shock following carotid artery cannulation, and then resuscitated. Control animals underwent carotid artery cannulation only (sham-shock). Bacterial translocation to the mesenteric lymph nodes, liver, or spleen was measured after 24 h. Transmucosal passage of fluorescein isothiocyanate (FITC)-labeled E. coli C-25, or FITC-conjugated LPS was measured in the Ussing chamber. Intestinal membranes were examined by light and confocal laser microscopy. Severe hemorrhagic shock resulted in a 60% mortality rate and a 100% incidence of bacterial translocation in surviving animals. Sham-shock rats had a 100% survival rate and a 33% incidence of bacterial translocation. Transmucosal passage of FITC-E. coli C-25 was similar in both groups; however, passage of FITC-LPS was never detected. Histologic analysis confirmed mucosal injury to the intestinal epithelium of rats subjected to severe hemorrhagic shock, and confocal laser microscopy demonstrated passage of FITC-E. coil C-25, but not of FITC-LPS across the ileal membranes. Disruption of the intestinal epithelium with a potent mucolytic agent did not result in significant increase in transmucosal passage of FITC-LPS. We conclude that pure LPS does not pass across the intestinal mucosa in vitro. Transmucosal passage of LPS in vivo may be due, at least in part, to the release of bacterial cell wall fragments containing LPS from killed bacteria that had previously translocated.

Animals↗
PubMed1998

Under the volcano: varieties of anger and their transformation.

This paper seeks to illustrate the ambiguity of the affect of 'anger' which masks a number of subtly different emotions observable in clinical work. The author differentiates between anger, rage and hatred in terms of the dialectical relationship between ego and self and pays particular attention to why it is that for some patients, experiences of anger may be harnessed creatively into development, whereas for others, they remain self destructive. Using illustrations from work with two patients in analysis, the author describes how a persistent grievance originating in the earliest stages of life is linked with hatred and can lead to a defensive self structure. It is suggested that the clues to the presence of a grievance and to its potential transformation are likely to be observable first in the analyst's countertransference in the form of an all-embracing emotional strait jacket. Analysts' capacity to tolerate their own hatred is crucial to the transformation of a patient's grievance.

Aggression↗
PubMed1996

Selective expression of c-mas proto-oncogene in rat cerebral endothelial cells.

Northern blot analysis of cultured endothelial cells derived from rat cerebral resistance vessels demonstrated the presence of c-mas mRNA. This is the first description of mas expression in non-neuronal cells. c-mas message was not detectable in cultured endothelial cells derived from other vascular beds, including rat aorta and mesenteric resistance vessels. Since c-mas has been purported to regulate the proliferation response to angiotensin, the growth properties of all three endothelial cell cultures were examined. The data indicated no differences in either basal or angiotensin-stimulated cell growth among brain, mesenteric or aortic-derived endothelial cells. These data suggest that c-mas is selectively expressed in brain endothelial cells and that this proto-oncogene does not regulate cell proliferation in this cell type.

Angiotensin II↗
PubMed1995

Molecular approaches to prevention and detection of epithelial ovarian cancer.

More than 90% of epithelial ovarian cancers arise from single cells. Malignant transformation can be associated with a number of molecular alterations including upregulation of tyrosine kinases and phosphatases, physiologic activation o ras, mutation of p53, amplification of myc, and increased activity of matrix metalloproteinases 2 and 9. Proliferation of transformed epithelial cells can be enhanced through the persistence of autocrine growth stimulation by TGF-alpha, loss of autocrine growth inhibition by TGF-beta, as well as paracrine growth stimulation by macrophage derived cytokines and OCAF, a novel lyso-phospholipid. Ascites tumor cells retain responsiveness to growth inhibition by TGF-beta which induces apoptosis in malignant ovarian epithelial cells, but not in normal ovarian surface epithelium. Proliferation of surface epithelial cells following ovulation may contribute to the pathogenesis of ovarian cancer. Use of oral contraceptives that suppress ovulation has been associated with reduced risk of ovarian cancer in later life. Retinoids also deserve further evaluation for chemoprevention. Treatment with fenretinide was associated with decreased incidence of ovarian cancer. Additive or synergistic inhibition of ovarian tumor cell proliferation has been observed with TGF-beta in combination with all-trans-retinoic acid. Early detection of ovarian cancer could improve survival. Transvaginal sonography (TVS) and serum markers such as CA-125 have been evaluated in multiple clinical trials. The former lacks adequate specificity, whereas the latter is not sufficiently sensitive. Use of multiple serum markers can improve sensitivity. A combination of CA-125, M-CSF and OVX-1 has detected > 95% of Stage I ovarian cancers. If similar results are obtained with different data sets, multiple serum markers could be used to trigger the performance of TVS, providing a potentially cost effective screening strategy. Prospective trials will be required to demonstrate that screening for early stage ovarian actually impacts on survival.

Diagnosis, Differential↗
PubMed1995

A randomized, double-blind, placebo-controlled trial of selective digestive decontamination in a medical-surgical intensive care unit.

A randomized, double-blind, placebo-controlled trial of selective decontamination of the oropharynx and gastrointestinal tract was conducted on 61 intubated patients in a medical-surgical intensive care unit (ICU) to determine the impact on nosocomial pneumonia, other infections, and emergence of colonization or infection with antibiotic-resistant bacteria. Over 8 months, 30 patients received an oral paste and solution containing polymyxin, gentamicin, and nystatin; 31 patients received a placebo paste and solution. At study entry, patients in both groups were seriously ill (mean acute physiologic score, 27.2), frequently had pulmonary infiltrates (73.8%), and were likely to be receiving systemic antibiotics (86.9%). There were no differences between study patients and control patients in these characteristics or in frequency of any nosocomial infection (50% vs. 55%), nosocomial pneumonia (27% vs. 26%), febrile days (2.3 vs. 2.0), duration of antibiotic therapy (14.0 vs. 13.4), or mortality rates (37% vs. 48%). There was no difference in infections caused by antibiotic-resistant gram-negative bacilli, although a trend towards more frequent infection with gentamicin-resistant enterococci was found for study patients. Selective decontamination did not appear to be effective in our very ill medical-surgical ICU patients, although the number of patients in our trial was sufficient to detect only a 50% or greater reduction in pneumonia rates.

Colistin↗