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Biomedical subjects

S Becker

Publications and source records attributed to S Becker.

At least 109 records · Page 6Linked to original sources
PubMed2000

Ambulatory surgery centers--current business and legal issues.

This article explores a handful of critical trends that have broad implications for ambulatory surgery centers and health care entities as a whole. As of the year 2000, the health care delivery system is experiencing broad changes and reconstruction in a variety of manners. One of the largest changes revolves around the accelerating movement of patient care from inpatient models to outpatient models, and the commensurate investment and development in outpatient systems and outpatient bricks and mortar. This metamorphosis is particularly evident as it relates to freestanding ambulatory surgery centers. This change in health care delivery will prove to have severe economic impacts on many of the nation's hospital systems.

Centers for Medicare and Medicaid Services, U.S.↗
PubMed2000

HCFA issues guidance and answers questions related to the provider-based status of facilities.

Over the last few years, the Health Care Financing Administration ("HCFA") has become increasingly concerned with hospital systems billing for services provided at related and affiliated sites as "provider-based" rather than independent facilities. By billing as provider-based, a hospital is entitled to charge HCFA in a slightly different manner that typically leads to higher reimbursement. In Program Memorandum to Intermediaries A-99-24, issued in May 1999, HCFA stated that, with the growth of integrated delivery systems, it has received numerous requests from entities requesting provider-based status. These requests, if approved, increase the portion of the facility's general and administrative costs supported by the Medicare program with no commensurate benefit to Medicare and its beneficiaries. Therefore, it is critical that HCFA designate as provider-based only those entities that are unquestionably qualified. On September 20, 2000, HCFA's administrator released a letter summarizing this concern over provider-based entities. The letter stated that the Department of Health and Human Services Office of Inspector General ("IG") has concluded that many hospital purchases of physician practices appear to have been designed not to ensure services are provided to participants in the most appropriate setting but, rather, simply to obtain higher Medicare payments. The IG strongly recommended that, if such arrangements continue, HCFA take steps to curtail them. The outcome of this recommendation is the proposed provider-based regulations ("Proposed Regulations") issued by HCFA on April 7, 2000.

Centers for Medicare and Medicaid Services, U.S.↗
PubMed1999

Immunologic and virologic studies in long-term nonprogressors with HIV-1 infection.

BACKGROUND: It is not known whether clinical latency in long-term nonprogressors (LTNP) with HIV-1 infection is due to a strong HIV-1 specific immune response of the host or to virologic factors. - METHODS: Peripheral blood mononuclear cells (PBMC) of 6 LTNP were analyzed for their phenotype, proliferation rates, natural killer (NK) cell activity, antibody dependent cellular cytotoxicity (ADCC), and CCR5 chemokine receptor genotype. Furthermore sequence analyses of the HIV-1 gene were performed. - RESULTS: Phenotypic analyses of lymphocyte subsets revealed increased CD8+ as well as HLA-DR+ expressing cells in LTNP and patients with progressive disease (PRO). Proliferation assays in LTNP and PRO showed a reduction of stimulation by polyclonal mitogens (PHA, ConA, PWM) of up to 60%. NK activity was within normal ranges in LTNP but reduced in PRO. 1 LTNP exhibited heterozygosity for CCR5-D32. A mutant HIV nef gene was not discovered by PCR in any of the LTNP. HIV-V3 loop PCR in 5 LTNP revealed the HIV-1B (NSI) subtype. In 2 patients further sequence analyses of the HIV-1 genome showed homozygous mutations in the Sp1 and NF-kB binding sites. CONCLUSION: The non-progression of HIV-1 infection in some LTNP seems to be due to single mutations in the viral genome resulting in a less replicative HIV-1 subtype or to a mutant chemokine receptor leading to a reduced HIV-1 entry into CD4+ cells. NK cell activity might be an additional contributing factor in controlling viremia.

Acquired Immunodeficiency Syndrome↗
PubMed1999

Exposure to urban air particulates alters the macrophage-mediated inflammatory response to respiratory viral infection.

Epidemiology studies associate increased pulmonary morbidity with episodes of high particulate air pollution (size range 0.1-10 microm diameter, PM10). Pneumonia, often viral in origin, is increased following episodes of high PM10 pollution. Therefore, this study was undertaken to investigate how PM10 alters airway inflammatory responses to respiratory syncytial virus (RSV), a frequent cause of viral pneumonia in infants and the elderly. Supernatants of unexposed and PM10-exposed alveolar macrophage (AM) cultured with uninfected or RSV-infected airway epithelial cells were assessed for a number of chemokines responsible for inflammatory responses in the lung. AM exposure to PM10 in the absence of infection resulted in a significant increase in interleukin (IL)-8 and macrophage inflammatory protein (MIP)-1alpha production but not in MIP-1beta or monocyte chemotactic protein (MCP)-1. AM responded to RSV infection by the production of IL-8, MIP-1alpha, MIP-1beta, and MCP-1, while RANTES was derived solely from the RSV-infected bronchial epithelial cell line BEAS-2B. In the presence of PM10, the AM response to RSV was blunted. RSV-induced MCP-1 was significantly decreased, and the levels of MIP-1 and IL-8 were lower than expected from a combined response to PM10 and RSV. Furthermore, AM analyzed for uptake of virus showed a 50% decrease in viral antigen when exposed to PM10 RSV-induced production of RANTES by epithelial cells was decreased in the presence of AM but not affected by PM10 exposure. Taken together, these results suggest that AM-regulated inflammatory responses to viral infection are altered by exposure to PM10 in a manner that may result in increased spread of infection and thus may increase viral pneumonia-related hospital admissions.

Adolescent↗
PubMed1999

Ambient air particles: effects on cellular oxidant radical generation in relation to particulate elemental chemistry.

Epidemiologic studies have reported causal relationships between exposures to high concentrations of ambient air particles (AAP) and increased morbidity in individuals with underlying respiratory problems. Polymorphonuclear leukocytes (PMN) are frequently present in the airways of individuals exposed to particles. Upon particulate stimulation the PMN may release reactive oxygen species (ROS), which can result in tissue damage and injury. In this study a wide range of AAP samples from divergent sources (1, natural dust; 2, oil fly ash; 2, coal fly ash; 5, ambient air; and 1, carbon black) were analyzed for elemental content and solubility in relation to their ability to generate ROS. Elemental analyses were carried out in AAP and dH(2)O-washed AAP using energy dispersive x-ray fluorescence (XRF). Percent of sample mass accounted for by XRF-detectable elements was 1.2% (carbon black); 22-29% (natural dust and ambient air particles); 13-22% (oil fly ash particles); 28-49% (coal fly ash particles). The major proportion of elements in most of these particles were aluminosilicates and insoluble iron, except oil-derived fly ash particles in which soluble vanadium and nickel were in highest concentrations, consistent with particle acidity as measured in the supernatants. Human blood-derived monocytes and PMN were exposed to AAP and dH(2)O-washed particles, and generation of ROS was determined using luminol-enhanced chemiluminescence (LCL) assay. All the particles induced chemiluminescence response in the cells, except carbon black. The oxidant response of monocytes induced by AAP (with the exception of oil fly ash particles) was less than the response elicited by PMN. The LCL response of PMN in general increased with all washed particles, with oil fly ash (OFA) and one urban air particle showing statistically significant (p < 0. 05) differences between dH(2)O-washed and unwashed particles. The LCL activity in PMN induced by both particles and dH(2)O-washed particles was significantly correlated with the insoluble Si, Fe, Mn, Ti, and Co content of particles (p < 0.05). No relationship between LCL activity in PMN and soluble transition metals such as V, Cr, Ni, and Cu was noted. Pretreatment of the particles with a metal ion-chelator, deferoxamine, did not affect LCL in PMN, suggesting that metal ions are not related to the induction of LCL in PMN. Particulate S content and acidity of the particles as measured in the supernatants did not relate to LCL activity in PMN. These results point to the possibility that the insoluble constituents of the particles are related to LCL in PMN. Since some of these dusts are capable of depositing in the lungs and can cause infiltration of PMN, the ability to activate those cells may contribute to particulate toxicity.

Air Pollutants↗
PubMed1999

Cytotoxicity and induction of proinflammatory cytokines from human monocytes exposed to fine (PM2.5) and coarse particles (PM10-2.5) in outdoor and indoor air.

Increased incidence of mortality and morbidity due to cardiopulmonary complications has been found to associate with elevated levels of particulate air pollution (particulate matter with an aerodynamic diameter < 10 microm, PM10 and <2.5 microm, PM2. 5). Lung injury and an imbalance of inflammatory mediators are proposed causative mechanisms, while the toxic constituents may be acidity, transition metals, organic, and biogenic materials. To compare the ability of inhalable fine particles (PM2.5), and coarse particles (PM10-2.5) to cause cell injury and cytokine production in monocytes, dichotomous Andersen samplers were used to collect size-fractionated PM10 for in vitro testing of the particle extracts. Particles from both outdoor and indoor air were collected onto Teflon filters, on nine separate occasions. Each filter was water extracted and each extract assessed for ability to cause cell death, as well as interleukin (IL)-6 and IL-8 production in human monocytes. Significant toxicity and cytokine production was induced by outdoor PM10-2.5, but not by outdoor PM2.5 or the particles collected indoors. Outdoor PM10-2.5 induced 20 times the amounts of IL-6 and IL-8 than the fine particles. Cytotoxicity was inhibited by deferoxamine, a chelator of transition metals, while cytokine production was not. On the other hand, lipopolysaccharide binding protein (LBP) completely inhibited cytokine induction by PM10-2.5, suggesting that gram-negative bacteria and/or endotoxins are components of PM10-2.5. The effective proinflammatory effects of endotoxin on macrophages may upset lung homeostasis while metals-induced cytotoxicity/necrosis may set up inflammation independent of macrophage-derived cytokines.

Acute-Phase Proteins↗
PubMed1999

The nucleoprotein of Marburg virus is target for multiple cellular kinases.

The nucleoprotein (NP) of Marburg virus is phosphorylated at serine and threonine residues in a ratio of 85:15, regardless of whether the protein is isolated from virions or from eukaryotic expression systems. Phosphotyrosine is absent. Although many potential phosphorylation sites are located in the N-terminal half of NP, this part of the protein is not phosphorylated. Analyses of phosphorylation state and phosphoamino acid content of truncated NPs expressed in HeLa cells using the vaccinia virus T7 expression system led to the identification of seven phosphorylated regions (region I*, amino acids 404-432; II*, amino acids 446-472; III*, amino acids 484-511; IV*, amino acids 534-543; V*, amino acid 549; VI*, amino acids 599-604; and VII*, amino acid 619) with a minimum of seven phosphorylated amino acid residues located in the C-terminal half of NP. All phosphothreonine residues and consensus recognition sequences for protein kinase CKII are located in regions I*-V*. Regions VI* and VII* contain only phosphoserine with three of four serine residues in consensus recognition motifs for proline-directed protein kinases. Mutagenesis of proline-adjacent serine residues to alanine or aspartic acid did not influence the function of NP in a reconstituted transcription/replication system; thus it is concluded that serine phosphorylation in the most C-terminal part of NP is not a regulatory factor in viral RNA synthesis.

Amino Acid Sequence↗
PubMed1999

Implicit learning in 3D object recognition: the importance of temporal context.

A novel architecture and set of learning rules for cortical self-organization is proposed. The model is based on the idea that multiple information channels can modulate one another's plasticity. Features learned from bottom-up information sources can thus be influenced by those learned from contextual pathways, and vice versa. A maximum likelihood cost function allows this scheme to be implemented in a biologically feasible, hierarchical neural circuit. In simulations of the model, we first demonstrate the utility of temporal context in modulating plasticity. The model learns a representation that categorizes people's faces according to identity, independent of viewpoint, by taking advantage of the temporal continuity in image sequences. In a second set of simulations, we add plasticity to the contextual stream and explore variations in the architecture. In this case, the model learns a two-tiered representation, starting with a coarse view-based clustering and proceeding to a finer clustering of more specific stimulus features. This model provides a tenable account of how people may perform 3D object recognition in a hierarchical, bottom-up fashion.

Animals↗
PubMed1999

Effect of nitrogen dioxide on respiratory viral infection in airway epithelial cells.

Nitrogen dioxide (NO(2)) is a common air pollutant outdoors and indoors in homes with unvented combustion sources. It is also a constituent of tobacco smoke. Epidemiological studies suggest that children exposed to NO(2), or living with smoking parents, have an increased incidence of respiratory viral infections. The most common virus causing severe respiratory symptoms in infants and young children is respiratory syncytial virus (RSV). In the present study we investigated whether NO(2) exposure affects RSV infection in airway epithelial cells, the host cells for viral replication and virus-induced cytokine production. Cultures of the bronchial epithelial cell line BEAS-2B exposed to 0.5, 1.0, and 1.5 ppm NO(2) for 60 min were infected with RSV. Viral replication, as well as RSV-induced interleukin (IL)-6 and IL-8, was assessed at various times postinfection. The NO(2) doses used were not toxic to the BEAS-2B cells as measured by release of lactic dehydrogenase (LDH). The internalization of RSV was increased by exposure to 0.5 ppm NO(2) and decreased by exposure to 1.5 ppm NO(2). On the other hand, the release of infectious virus 48 h postexposure was not affected by the two lower doses of NO(2), but was significantly reduced in cells exposed to 1.5 ppm NO(2). Virus-induced cytokine production was also significantly reduced in cells exposed to 1.5 ppm NO(2), and not affected by 0.5 and 1.0 ppm. It is likely that the decrease in cytokine production is related to the decrease in viral burden. These data suggest that possible increases in viral clinical symptoms associated with NO(2) may not be caused by increased susceptibility of the epithelial cells to infection but may result from effects of NO(2) on host defenses that prevent the spread of virus.

Air Pollutants↗