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Biomedical subjects

C Wiener

Publications and source records attributed to C Wiener.

14 recordsLinked to original sources
PubMed1997

Structural and functional analysis of hypoxia-inducible factor 1.

Hypoxia-inducible factor 1 (HIF-1) is a basic helix-loop-helix protein that activates transcription of hypoxia-inducible genes, including those encoding: erythropoietin, vascular endothelial growth factor, heme oxygenase-1, inducible nitric oxide synthase, and the glycolytic enzymes aldolase A, enolase 1, lactate dehydrogenase A, phosphofructokinase I, and phosphoglycerate kinase 1. Hypoxia response elements from these genes consist of a HIF-1 binding site (that contains the core sequence 5'-CGTG-3') as well as additional DNA sequences that are required for function, which in some elements include a second HIF-1 binding site. HIF-1 is a heterodimer. The HIF-1 alpha subunit is unique to HIF-1, whereas HIF-1 beta (ARNT) can dimerize with other bHLH-PAS proteins. Structural analysis of HIF-1 alpha revealed that dimerization with HIF-1 beta (ARNT) requires the HLH and PAS domains, DNA binding is mediated by the basic domain, and that HIF-1 alpha contains a carboxyl-terminal transactivation domain. Co-transfection of HIF-1 alpha and HIF-1 beta (ARNT) expression vectors and a reporter gene containing a wild-type hypoxia response element resulted in increased transcription in non-hypoxic cells and a superinduction of transcription in hypoxic cells, whereas HIF-1 expression vectors had no effect on the transcription of reporter genes containing a mutation in the HIF-1 binding site. HIF-1 alpha and HIF-1 beta (ARNT) protein levels were induced by hypoxia in all primary and transformed cell lines examined. In HeLa cells, the levels of HIF-1 alpha and HIF-1 beta protein and HIF-1 DNA-binding activity increased exponentially as cellular oxygen tension decreased, with maximum values at 0.5% oxygen and half-maximal values at 1.5 to 2% oxygen. HIF-1 alpha and HIF-1 beta (ARNT) mRNAs were detected in all human, mouse, and rat organs assayed and mRNA expression was modestly induced in rodents subjected to hypoxia. HIF-1 alpha protein levels were induced in vivo when animals were subjected to anemia or hypoxia. The HIF1A gene was mapped to human chromosome 14q21-q24 and mouse chromosome 12.

Animals↗
PubMed1996

Is there an occupational etiology of inverted papilloma of the nose and sinuses?

The etiology of inverted papilloma is believed to be of viral origin, as viruses or viral material is found in these tumors of the nose and paranasal sinuses. As the nose is the first defense line of the respiratory tract, we suspected an etiology of airborne pollution as well, especially occupational pollution. We examined a group of 47 patients treated in our department for nasal inverted papilloma, asking about lifelong professional history and occupational exposure. A matched control group of patients with non-malignant diseases was included in the study. We found a significantly higher degree of occupational exposure to different smokes, dusts, and aerosols in the case group. No similar results have been published to our knowledge. To obtain better proof of the role of possible noxious agents, a study technically investigating exposure is mandatory.

Case-Control Studies↗
PubMed1989

Untrained, unpaid, and unacknowledged: the patient as worker.

This article considers the patient as the central worker in his or her own care. It traces the history of a concept called "illness trajectory," explaining how this concept has been questioned, reformulated, and expanded through research among people with chronic illness. The trajectory concept illuminates the manner in which living with a chronic illness imposes on-the-job training on the unskilled patient as worker, who must learn to integrate biographical work, illness-related work, and everyday life work. That this patient work is unpaid renders it invisible to a society accustomed to valuing work only as it is connected to monetary exchange. Finally, by virtue of this invisible dimension, the work patients do remains unacknowledged and unappreciated by the larger society.

Chronic Disease↗
PubMed1982

The work of hospitalized patients.

Patient's participation in their own care, conceived as work, is the central theme of this paper. A second theme is the patients' work in relation to technology. A third is: the prevalence of chronic illness and how this relates to patients' work in the service of their own care. Data are from a multi-hospital field-research and interviewing study of technology and patients care, carried out in San Francisco and the Bay Area, California. Questions addressed in this paper include the following: What are the sources of patients' work? What types of work do patients do? How does that work relate to courses of illness and the phases? What is the relation of that work to staff work? Under what conditions is the work visible or invisible to staff? Under what conditions is the work appreciated or not by staff? What are some consequences of patient work for staff work, for the management of the courses of illness, and for the patients' own medical and biographical fates? How does patient work at the hospital relate to patient work done at home?

California↗
PubMed1982

Sentimental work in the technologized hospital.

Sentiment is frequently involved in work either to get work done efficiently or because of humanistic considerations. This paper explores several questions: Are there different kinds of sentimental work? How is sentimental work carried out? When and where is it done; when not? Who does it? What is its relation to other types of work? When is it likely to be in focus for the workers? When is it visible, when invisible and to whom? What are its consequences: for work, staff, client and organization? The illustrative materials used in this paper are taken from research on the impact of technology on medical work in hospitals.

Affect↗
PubMedDate not supplied

Metabolism and disposition of 1,4,7,8-tetrachlorodibenzo-p-dioxin in rats.

Metabolism studies of 1,4,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a relatively nontoxic dioxin congener, were undertaken to gain a better understanding of mammalian metabolism of dioxins without the problems associated with the use of the most toxic congener, 2,3,7,8-TCDD. 14C-1,4,7,8-TCDD was dosed to conventional and bile-cannulated rats at a level of 8 mg/kg. The 14C was excreted almost entirely in 72 hours with the major routes of excretion feces and bile. Metabolites were identified from the feces, bile, and urine by GC-MS or negative ion FAB MS and 1H NMR. The two major fecal metabolites were hydroxylated tetra- and triCDDs. Glucuronide and sulfate conjugates of these hydroxyl metabolites were found in the urine and bile. Minor metabolites included dichlorocatechol, dihydroxylated tetra- and triCDDs, and conjugates of these compounds.

Animals↗