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The inverse problem of the identification of an anomalous object (e.g., cyst or tumor) in a female breast immersed in water is solved by the matching of theoretical fields (for trial objects), employing an approximate field ansatz, to the scattered ultrasonic wave field measured on a surface fully enclosing the object.
The number of potentially intimate relationships between brain tumors and the precursor cells that contribute to normal central nervous system (CNS) development and repair now appears to be somewhat larger than would have been anticipated only a few years ago. It also appears that understanding the vulnerabilities of CNS precursor cells, and of the specific cells that they generate, might help us to reveal the biological basis for the cognitive impairment that is increasingly recognized as an adverse effect of systemic cancer therapies. Using neural stem cells as therapeutic vehicles in the treatment of brain tumors could be modified to allow repair of the damage caused by brain tumors themselves and of the neurological impairment that is frequently associated with traditional cancer treatment approaches.
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The many parties, which now possess a role in behavioral health care services, are each concerned about the quality of these services. The concept of accreditation of MBHOs differs little from the board certification and licensure mechanisms used to ensure a minimal standard of care among practitioners. In the same way that behavioral health patients use licensure to seek competent providers, payers use accreditation as a way to ensure that MBHOs, given the task of cost control, are also active in ensuring that cost containment does not translate into decreased quality of care. Accreditation has established standards that fundamentally require MBHOs to implement QI programs directed at assessing and implementing efforts to improve care on a systemic level. NCQA accreditation of MBHOs reflects an effort to both regulate a novel industry as well as establish standards that reflect an ideal of health care. Currently, relatively few MBHOs receive full accreditation. This suggests that NCQA maintains its ideals but also that many MBHOs do not have the quality improvement programs that adequately demonstrate an interest in assessing and improving upon continuity and population-based quality care. As a fledgling industry, MBHOs are subject to unique market demands and trial and error. These forces have alienated many practitioners who provide services to MBHO members; however, practitioners must be able to tease out those aspects of managed care that facilitate quality care for their patients. Fundamental to this is the need for practitioners to understand and contribute meaningfully to QI initiatives directed at meeting NCQA standards. Despite their impositions, the new demands they place on practitioners, and the conflicted relationship in which they take place, QI efforts reflect an effort on the part of accrediting organizations and MBHOs to define, through empirical assessment and improvement efforts, quality care at a systemic level. Such care directly relates to effective behavioral health care by ensuring that a population of members receives care over a continuum of time and setting. Accreditation standards ultimately translate into quality of care and service, which patients and practitioners as well as the other stakeholders in the health care marketplace, agree is important.
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Angioimmunoblastic lymphadenopathy (AIL) still is a clinico-pathological syndrome with little known physiopathology. The advent of molecular biology has improved our understanding of this syndrome by characterization of the clonal cell. With this technique, combined with cytogenetics and immunohistochemistry, three pathological states have been individualized: 1) true AIL without evidence of monoclonal proliferation; 2) transformed AIL, and 3) AIL-like T-cell lymphoma. This clinical complex can be integrated in an evolutive continuum, starting with simple lymphoid hyperplasia and ending with frank malignant T-cell lymphoma.
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Over the past two decades, the applications of genetic and genomic technologies have begun to transform research questions and practices within epidemiology and toxicology, the "core sciences" of public health (Annu. Rev. Public Health 21 (2000) 1). These technologies provide new models and techniques for studying genetic traits, environmental exposures, and gene-environment interaction in the production of human health and illness. This paper explores the consequences of emergent genetic and genomic approaches, their ongoing redefinitions of both genetic and environmental "risks", and their potential implications for public health practice. The central argument of the paper is that the increasing focus on gene-environment interaction directs scientific, biomedical, and public health attention both inward, to the gene/genome, and outward, to particular places. In so doing, studies of gene-environment interaction create a challenging and productive tension-at the same time that bodies are being geneticized (Am. J. Law Med. 17 (1992) 15), they also are emphatically emplaced, located where social and cultural practices come to matter. This tension, this simultaneous movement outward and inward, towards the gene and towards the environment, into the body and into place, opens up a vista into the processes through which culture and biology form a locally and historically situated dialectic (Encounters With Aging: Mythologies of Menopause in Japan and North America, University of California Press, Berkeley, CA, 1993) and raises important questions about the production of health and illness.
Use or abuse of licit and illicit substances is often associated with environmental stress. Current clinical evidence clearly demonstrates neurobehavioral, somatic growth and developmental deficits in children born to drug-using mothers. However, the effects of environmental stress and its interaction with prenatal drug exposure on a child's development is unknown. Studies in pregnant animals under controlled conditions show drug-induced long-term alterations in brain structures and functions of the offspring. These cytoarchitecture alterations in the brain are often associated with perturbations in neurotransmitter systems that are intimately involved in the regulation of the stress responses. Similar abnormalities have been observed in the brains of animals exposed to other adverse exogenous (e.g., environmental stress) and/or endogenous (e.g., glucocorticoids) experiences during early life. The goal of this article is to: (1) provide evidence and a perspective that common neural systems are influenced during development both by perinatal drug exposure and early stress exposure; and (2) identify gaps and encourage new research examining the effects of early stress and perinatal drug exposure, in animal models, that would elucidate how stress- and drug-induced perturbations in neural systems influence later vulnerability to abused drugs in adult offspring.
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Hemochromatosis is a genetic disease of iron overload due to intestinal hyperabsorption of iron. It is one of the most prevalent autosomal recessive diseases in Caucasian populations. Hemochromatosis causes severe visceral and metabolic complications at adulthood, which include cirrhosis, diabetes, arthropathy and cardiac failure. A major breakthrough has been the discovery, in 1996, of the HFE gene which is strongly associated with the phenotypic expression of the disease. This discovery has, very quickly, provided a powerful genetic blood test which permits, in most cases, to establish the diagnosis in a non invasive way (i.e. without a liver biopsy). Hemochromatosis can be cured by repeated venesections provided the diagnosis has been detected sufficiently early. Moreover, an efficient preventive strategy can be applied to family members and should now be proposed to the general population. Finally, the identification of the HFE gene has paved the way for the identification of new iron overload entities.
A bacterial housekeeping function, which requires both recombination and replication enzymes, has been identified that re-establishes inactivated replication forks under normal growth conditions. Some long-tract gene-conversion events initiated by double-strand breaks in yeast and mammalian cells can be attributed to recombination-directed DNA replication. Double-strand break repair in yeast has been shown to require both leading- and lagging-strand DNA synthesis. These observations suggest that the recombination and replication machinery cooperate to maintain genomic integrity.
Stress and mitogens stimulate overlapping sets of MAP kinases in mammalian cells; MAP kinase pathways appear more distinct in yeast, but differences between the two systems may be less than is presently evident.
Clathrin-mediated endocytosis is the major mechanism by which proteins and membrane lipids gain access into cells. Over the past several years, an array of proteins has been identified that define the molecular machinery regulating the formation of clathrin-coated pits and vesicles. This article focuses on how the identification of this machinery has begun to reveal a molecular basis for a link between endocytosis and the actin cytoskeleton--a link that had long been suspected to exist in mammalian cells but which had remained elusive. In particular, I discuss the relationship between actin and three components of the endocytic machinery--dynamin, HIPs (huntingtin-interacting proteins) and intersectin.
While many people view the war on abortion and the war on drugs on the part of state and federal governments in the USA as distinct, there are in fact many connections and a great deal of overlap between the two. Their histories, the strategies used to control and punish certain reproductive choices and those to control the use of certain drugs, the limitations that are placed on access to abortion and other reproductive health care and drug treatment, and the populations most harmed by those limitations are remarkably similar. These similarities are particularly apparent where the issues coalesce in the regulation and punishment of pregnant, drug-using women [1]. Efforts to control reproduction and drugs are rooted in forms of bigotry and prejudice that are essentially the same; African-American women are particularly harmed by them [2]. These efforts reflect a common political agenda and draw attention away from real underlying issues, including poverty, race discrimination and lack of a coherent national health care policy. Those who fight against each of them must recognize that they have a common cause and need a comprehensive strategy to address both as fundamental issues of social justice.
Antigenic peptides are translocated by the TAP peptide transporter from the cytosol into the endoplasmic reticulum (ER) for loading onto MHC class I molecules. Peptides that fail to bind need to be removed from the ER. Here we provide evidence that peptide export utilizes the Sec61p translocon as demonstrated by blocking this channel with bacterial exotoxin. Peptide export interferes with the retrotranslocation of beta2-microglobulin from the ER to the cytosol, suggesting similar pathways for the disposal of proteins and oligopeptides. Peptide export requires ATP supply to the ER lumen but is independent of ATP hydrolysis.