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PubMed2006

The difference between drug money and a "lifetime's savings".

In many countries, monies suspected of being associated with drug trafficking can be seized by the authorities. One of the ways of investigating this association is through the analysis of seized banknotes for traces of controlled drugs. We report three studies which may assist the expert in assessing whether banknotes contaminated with diamorphine are part of the general population of notes in circulation or whether they show unusual contamination patterns which require explanation. Study 1 is based on three plausible contamination scenarios as they may occur during the various stages of an illicit drug transaction and seizure. It shows that notes which have been in direct contact with visible traces of diamorphine show significantly higher contamination to those in more indirect contact with the drug. Study 2 investigates the transfer of diamorphine from one highly contaminated note to other notes in a bundle over a period of 10 weeks with and without agitation. It was found that the total amount of drug transferred was smaller than 6% and no more than 4 out of a bundle of 10 previously clean notes became lightly contaminated. Based on extensive background data, study 3 proposes a probabilistic model to assess whether an observed proportion of diamorphine bearing banknotes is likely to have been contaminated by chance. The model predicts that there is only a 0.3% chance that a bundle of 100 notes from the general banknote population contains more than six contaminated specimens. Jointly, the three studies give useful indications for the spread of contamination throughout a sample and the amounts of heroin which may be expected given plausible contamination scenarios.

Journal Article↗
PubMed1997

MHC class II deficiency: definition of a new complementation group.

MHC class II deficiency is a severe primary immunodeficiency characterized by the absence of Major Histocompatibility Complex class II gene expression. It is genetically heterogenous and can result from defects in several different transacting regulatory factors required for transcription of MHC class II genes. Cell lines from MHC class II deficiency patients have been assigned to three complementation groups (A, B, C). An in vitro generated cell line (6.1.6) was reported to be the sole representative of a fourth group (group D). The molecular defect in 6.1.6 resides in the recently cloned RFXAP gene. Direct complementation experiments and mutation analysis were performed with cell lines from several MHC class II deficiency patients in which the affected gene had not been identified. These experiments have allowed us to define a previously unrecognized MHC class II deficiency complementation group containing patients having mutations in the RFXAP gene.

Animals↗
PubMed1998

What matters? What does not? Five perspectives on the association between marital transitions and children's adjustment.

This article presents an analysis of 5 views of factors that contribute to the adjustment of children in divorced families or stepfamilies. These perspectives are those that emphasize (a) individual vulnerability and risk; (b) family composition; (c) stress, including socioeconomic disadvantage; (d) parental distress; and (e) disrupted family process. It is concluded that all of these factors contribute to children's adjustment in divorced and remarried families and that a transactional model examining multiple trajectories of interacting risk and protective factors is the most fruitful in predicting the well-being of children.

Adaptation, Psychological↗
PubMed1995

Health care contracts in Britain and the United States: a case for technology transfer?

One unexpected point of convergence between the British and North American health care systems is the increased use of negotiated contracts to govern relationships between purchasers and providers. In Britain, the internal market reforms introduced a special regime of National Health Service (NHS) contracts; in the United States there has been a move from disorganization towards integration with the emergence of larger purchasing coalitions and provider organizations. While, in the past, US patients were simply billed for services or assigned claims to the provider, it is now common for payment to be made directly from purchaser to provider and for the terms of these transactions to be set out in contracts. This paper draws on the reading of contracts, interviews with contracting parties, and ongoing research on NHS contracting in Wales to compare contracting practice within the two systems. It examines how the very different environments of the public, hierarchically-regulated NHS and the private health care market of the US influence the detailed content of contract clauses. The analysis passes over similarities, different solutions to common problems, and fundamental differences of approach, before considering the possibilities for transfers of contracting 'technology'.

Contract Services↗
PubMed2005

Dialysis facility joint ventures--current structures and issues.

With the ongoing consolidation of the health care industry, including renal care, providers and physicians alike are using joint ventures as a means to partner on business transactions. This article discusses the expanding use of joint ventures in health care, including the dialysis industry, and looks at the types of structures being utilized and key legal concerns relating to such structures and issues.

Cost-Benefit Analysis↗
PubMed1999

Phenotype-dependent expression of alpha-smooth muscle actin in visceral smooth muscle cells.

Alpha-Smooth muscle actin is one of the molecular markers for a phenotype of vascular smooth muscle cells, because the actin is a major isoform expressed in vascular smooth muscle cells and its expression is upregulated during differentiation. Here, we first demonstrate that the phenotype-dependent expression of this actin in visceral smooth muscles is quite opposite to that in vascular smooth muscles. This actin isoform is not expressed in adult chicken visceral smooth muscles including gizzard, trachea, and intestine except for the inner layer of intestinal muscle layers, whereas its expression is clearly detected in these visceral smooth muscles at early stages of the embryo (10-day-old embryo) and is developmentally downregulated. In cultured gizzard smooth muscle cells maintaining a differentiated phenotype, alpha-smooth muscle actin is not detected while its expression dramatically increases during serum-induced dedifferentiation. Promoter analysis reveals that a sequence (-238 to -219) in the promoter region of this actin gene acts as a novel negative cis-element. In conclusion, the phenotype-dependent expression of alpha-smooth muscle actin would be regulated by the sum of the cooperative contributions of the negative element and well-characterized positive elements, purine-rich motif, and CArG boxes and their respective transacting factors.

Actins↗
PubMed1999

Extinction of alpha1-antitrypsin expression in cell hybrids is independent of HNF1alpha and HNF4 and involves both promoter and internal DNA sequences.

In rat hepatoma x fibroblast somatic cell hybrids, extinction of rat alpha1-antitrypsin (alpha1AT) gene expression is accompanied by the loss of liver-enriched transcription factors hepatocyte nuclear factor 1 (HNF1alpha) and hepatocyte nuclear factor 4 (HNF4). Previous analysis showed that forced expression of functional HNF1alpha failed to prevent extinction of the rat alpha1AT locus in cell hybrids. Here I show that ectopic co-expression of HNF1alpha plus HNF4 fails to prevent extinction of either rat or human alpha1AT genes in cell hybrids. A 40 kb human alpha1AT minilocus integrated into the rat genome is fully silenced in cell hybrids in the presence of transacting factors. The integrated alpha1AT promoter, but not a viral or ubiquitously active promoter, is repressed 35-fold in the cell hybrids. In addition, position effects also contributed to extinction of many integrated transgenes in a cell type-dependent manner. Finally, internal DNA sequences within the human alpha1AT gene contributed dramatically to the extinction phenotype, resulting in a further 10- to 30-fold reduction in alpha1AT gene expression in cell hybrids. Thus, multiple mechanisms contribute to silencing of tissue-specific gene expression of the alpha1AT gene in cell hybrids.

Animals↗
PubMed1995

Human T-cell leukemia virus type I tax transactivates the interleukin-6 gene in human rheumatoid synovial cells.

OBJECTIVE: To determine the effect of the human T cell leukemia virus type I (HTLV-I) tax gene on interleukin-6 (IL-6) production and gene transcription in synovial cells, we established the synovial cell line, E-11, from a patient with rheumatoid arthritis. METHODS: E-11 cells were transfected with tax expression vector using the calcium phosphate coprecipitation method. IL-6 production and gene expression were investigated by ELISA and Northern blot analysis, respectively. To clarify how tax induces IL-6 gene expression, we used deletion analysis and chloramphenicol acetyltransferase (CAT) assay, and electrophoretic mobility shift assay (EMSA). RESULTS: Transfection of the tax gene induced markedly high levels of IL-6 mRNA. Furthermore, the tax gene strongly transactivated IL-6 gene promoter activity assayed by CAT assay. By using deletion and site specific mutations, we have identified a nuclear factor (NF)-kappa B sequence (positions -73 to -63) which is essential for tax transaction. EMSA demonstrated the induction of specific binding of nuclear extracts to the NF-kappa B sequence by HTLV-I tax. CONCLUSION: The HTLV-1 tax gene may transactivate IL-6 gene in the synovial cells through NF-kappa B and may contribute in the pathophysiology of HTLV-I associated arthritis.

Arthritis, Rheumatoid↗
PubMed1994

Depression and the social developmental context of adolescence.

This article examines the interrelations of personal and social factors in fostering longitudinal patterns of depressive symptoms, using 3 waves of data from high school students in the Boston area. Previously depressed and nondepressed youths differed markedly in their emotional responsiveness to family and friend relations. Chronically depressed youths were unresponsive to family problems, but were highly reactive to peer relations. Among previously asymptomatic youths, family relations exerted greater effects on depressed mood than relations with peers. Further analyses suggest a process through which chronic family turmoil shapes long-term mental health while also intensifying the distancing from family and investment in peer relationships that typically occurs in adolescence. Findings illustrate the importance of modeling transactions between personal and environmental factors in research on adolescent mental health and development.

Adolescent↗
PubMed1997

Components of the costs of controlling quality: a transaction cost economics approach.

This article identifies the components that contribute to a healthcare organization's costs in controlling quality. A central tenet of our argument is that at its core, quality is the result of a series of transactions among members of a diverse network. Transaction cost economics is applied internally to analyze intraorganizational transactions that contribute to quality control, and questions for future research are posed.

Cost Allocation↗
PubMed2005

Ecological theory in practice: illustrations from a community-based intervention to promote the health of recent mothers.

We present a qualitative case study where we used four principles of ecological theory from community psychology as a template to assess the dynamics about how a preventive community intervention was transacted in eight communities in Victoria, Australia. The principles were cycling of resources, interdependence, adaptation, and succession. Ecological thinking focuses on key resources in communities. That is, the people, events, and settings that are the foundations of thinking about communities as systems. The data set consists of field diaries kept by and serial interviews with nine community development workers over a 2-year period. We found that the analysis highlighted a process-oriented way of representing the intervention, one that sees beyond the intervention's technical components (or packaged elements) to the complexities of the cultural and political change processes occurring beneath. The value of this is the attention focussed on likely project sustainability.

Community Networks↗
PubMed2006

Nrf1 is targeted to the endoplasmic reticulum membrane by an N-terminal transmembrane domain. Inhibition of nuclear translocation and transacting function.

Expression of antioxidant and phase 2 xenobiotic metabolizing enzyme genes is regulated through cis-acting sequences known as antioxidant response elements. Transcriptional activation through the antioxidant response elements involves members of the CNC (Cap 'n' Collar) family of basic leucine zipper proteins including Nrf1 and Nrf2. Nrf2 activity is regulated by Keap1-mediated compartmentalization in the cell. Given the structural similarities between Nrf1 and Nrf2, we sought to investigate whether Nrf1 activity is regulated similarly to Nrf2. Nrf1 also resides normally in the cytoplasm of cells. Cytoplasmic localization however, is independent of Keap1. Colocalization analysis using green fluorescent protein-tagged Nrf1 and subcellular fractionation of endogenous Nrf1 and fusion proteins indicate that Nrf1 is primarily a membrane-bound protein localized in the endoplasmic reticulum. Membrane targeting is mediated by the N terminus of the Nrf1 protein that contains a predicted transmembrane domain, and deletion of this domain resulted in a predominantly nuclear localization of Nrf1 that significantly increased the activation of reporter gene expression. Treatment with tunicamycin, an endoplasmic reticulum stress inducer, caused an accumulation of a smaller form of Nrf1 that correlated with detection of Nrf1 in the nucleus by biochemical fractionation and immunofluorescent analysis. These results suggest that Nrf1 is normally targeted to the endoplasmic reticulum membrane and that endoplasmic reticulum stress may play a role in modulating Nrf1 function as a transcriptional activator.

Amino Acid Sequence↗
PubMed1991

Social support as a double-edged sword: the relation of positive and problematic support to depression among rheumatoid arthritis patients.

This study considers social network interactions as a potential source of both stress and support for individuals coping with a chronic illness. The sample consisted of 101 recently-diagnosed rheumatoid arthritis patients. Symptoms of depression were assessed using the Center for Epidemiologic Studies Depression scale. Hierarchical multiple regression analyses examined the conjoint effects of social support and problematic interactions on symptoms of depression. Receipt of positive or helpful support from close friends and family was related to lower depression; receipt of problematic support was related to increased depression. A positive x problematic support interaction suggested that the costs of problematic support do not cancel out the benefits of positive support. Patients who reported both little support and a greater degree of problematic interactions experienced the highest level of symptoms. The findings emphasize the need to consider positive and negative aspects of support transactions conjointly in assessing their stress-reducing and health-protective potential.

Adaptation, Psychological↗
PubMed2005

Private obstetric practice in a public hospital: mythical trust in obstetric care.

There is evidence to suggest the decline of trusting relationships in modern healthcare systems. The primary aim of this study was to investigate the role of trust in medical transactions in Thailand, using obstetric care as a tracer service. The paper proposes an explanatory framework of trust for further investigation in other healthcare settings. The study site was a 1300-bed tertiary public hospital in Bangkok which it provides two forms of obstetric care: regular obstetric practice (RP) and private obstetric practice (PP). Forty pregnant women were selected and interviewed using a set of guiding questions. A thematic analysis of the interviews was undertaken to generate understanding and develop an explanatory framework. It was found that patients' trust in obstetric services was influenced by their perceptions of risk and uncertainty in pregnancy and childbirth, and that these perceptions were linked to their social class. Social class also influenced the accessibility and affordability of care to patients. Middle class pregnant women with relatively high-level concerns about risk and uncertainty preferred using PP service as a means to achieve interpersonal trust. These women thought that an informal payment would provide the basis for interpersonal trust between themselves and the chosen obstetricians. In practice, however, obstetricians involved in PP rarely acknowledged this reciprocal relationship and hardly expressed the additional courtesy expected by patients. As a result, PP service only created an expensive impersonal trust that was mistaken as interpersonal trust by patients. Negative outcomes from PP often caused disappointment that could eventually lead to medical litigation. The study suggests that there are some negative impacts of PP within the health system. Negative experiences among PP users may undermine trust not only in the specific doctor but also trust in health professionals and hospitals more generally. Steps need to be undertaken to protect and strengthen existing impersonal trust, which combine institutional trust based on good governance and service quality with trust in the professional standard of practice. The explanatory framework developed through this study provides a foundation for further studies of trust in different specialties and care settings.

Adult↗
PubMed2003

delta-Globin gene structure and expression in the K562 cell line.

The delta-globin gene produces the delta chain of Hb A2 which represents less than 3% of the hemoglobin (Hb) in normal individuals. The delta-globin gene is also expressed in the human erythroleukemia cell line K562. The expression of the delta-globin gene in this cell line is unexpected since K562 shows an embryonic-fetal globin gene expression pattern with no expression of the adult beta-globin gene. delta-Globin gene activation has been proposed as a potential therapeutic tool for the cure of delta-thalassemia (thal). In order to shed some light on the delta-globin gene activation in K562 the present study has: (1) determined the complete nucleotide sequence of the delta- and beta-globin genes; (2) assessed, by reverse transcription-polymerase chain reaction (RT-PCR), the relative delta- and beta-globin mRNA level; and (3) analyzed the exact level of the endogenous expression delta-globin gene by S1 mapping. No sequence variations were identified in the (delta- and beta-globin genes when compared to the normal sequences. delta-Globin mRNA represent more than 95% of the total delta + beta-mRNA content. The level of expression of the delta-globin gene is 12.3% (+/- 1.2) compared to the endogenous alpha-globin gene. These results indicate that the high expression of the delta-globin gene in K562 is most likely due to the transacting environment. Therefore, the presence and/or absence of specific transacting factors are able to specifically activate the human delta-globin gene. The level of expression of the delta-globin gene in this cell line suggests that it could be of relevance to identify the transacting factor(s) responsible for this selective activation in order to better understand the molecular mechanisms undergoing gene activation.

Gene Expression Regulation↗
PubMed2003

And you thought you were done with HIPAA: complying with the new security rule.

On February 20, 2003, the Department of Health and Human Services (HHS), pursuant to its authority under the Health Insurance Portability and Accountability Act of 1996 (HIPAA), issued the final rule on Security Standards for electronic protected health information (PHI). The rule addresses the duties of providers who conduct electronic transactions covered under the HIPAA transactions and code sets rule to address the security issues surrounding the storage and transmission of electronic PHI. Providers who are required to comply with the security rule must do so by April 20, 2005. While this may seem like a long time, the compliance requirements are lengthy and burdensome, so providers would be well advised to start compliance efforts now. Appointing a security officer and beginning a risk analysis should be the first priorities of any practice. While the security officer will be integral in a practice's compliance, it is ultimately the burden of the practice to ensure compliance with the rule. Penalties for non-compliance are stiff: civil money penalties of up to a $100 fine for every violation of each requirement or prohibition, capped at $25,000 per year for all violations of an identical requirement or prohibition. Criminal penalties must be imposed if a person knowingly and in violation of the security rule: obtains individually identifiable health information relating to an individual or discloses individually identifiable information to another person. This article is not, and should not be construed as, legal advice or an opinion on specific situations.

Journal Article↗
PubMed2006

Unraveling the 'DEAD-box' helicases of Plasmodium falciparum.

The causative agent for the most fatal form of malaria, Plasmodium falciparum, has developed insecticide and drug resistance with time. Therefore combating this disease is becoming increasingly difficult and this calls for finding alternate ways to control malaria. One of the feasible ways could be to find out inhibitors/drugs specific for the indispensable enzymes of malaria parasite such as helicases. These helicases, which contain intrinsic nucleic acid-dependent ATPase activity, are capable of enzymatically unwinding energetically stable duplex nucleic acids into single-stranded templates and are required for all the nucleic acid transactions. Most of the helicases contain a set of nine extremely conserved amino acid sequences, which are called 'helicase motifs'. Due to the presence of the DEAD (Asp-Glu-Ala-Asp) in one of the conserved motifs, this family is also known as the 'DEAD-box' family. In this review, using bioinformatic approach, we describe the 'DEAD-box' helicases of malaria parasite P. falciparum. An in depth analysis shows that the parasite contains 22 full-length genes, some of which are homologues of well-characterized helicases of this family from other organisms. Recently we have cloned and characterized the first member of this family, which is a homologue of p68 and is expressed during the schizont stage of the development of the parasite [Pradhan, A., Chauhan, V.S., Tuteja, R., 2005a. A novel 'DEAD-box' DNA helicase from Plasmodium falciparum is homologous to p68. Mol. Biochem. Parasitol. 140, 55-60.; Pradhan A., Chauhan V.S., Tuteja R., 2005b. Plasmodium falciparum DNA helicase 60 is a schizont stage specific, bipolar and dual helicase stimulated by PKC phosphorylation. Mol. Biochem. Parasitol. 144, 133-141.]. It will be really interesting to clone and characterize other members of the 'DEAD-box' family and understand their role in the replication and transmission of the parasite. These detailed studies may help to identify a parasite-specific enzyme, which could be a potential drug target to treat malaria. The various steps at which this probable drug can act are also discussed.

Animals↗
PubMed1998

Alpha-thalassaemia.

alpha-Thalassaemias are genetic defects extremely frequent in some populations and are characterized by the decrease or complete suppression of alpha-globin polypeptide chains. The gene cluster, which codes for and controls the production of these polypeptides, maps near the telomere of the short arm of chromosome 16, within a G + C rich and early-replicating DNA region. The genes expressed during the embryonic (zeta) or fetal and adult stage (alpha 2 and alpha 1) can be modified by point mutations which affect either the processing-translation of mRNA or make the polypeptide chains extremely unstable. Much more frequent are the deletions of variable size (from approximately 3 to more than 100 kb) which remove one or both alpha genes in cis or even the whole gene cluster. Deletions of a single gene are the result of unequal pairing during meiosis, followed by reciprocal recombination. These unequal cross-overs, which produce also alpha gene triplications and quadruplications, are made possible by the high degree of homology of the two alpha genes and of their flanking sequences. Other deletions involving one or more genes are due to recombinations which have taken place within non-homologous regions (illegitimate recombinations) or in DNA segments whose homology is limited to very short sequences. Particularly interesting are the deletions which eliminate large DNA areas 5' of zeta or of both alpha genes. These deletions do not include the structural genes but, nevertheless, suppress completely their expression. Larger deletions involving the tip of the short arm of chromosome 16 by truncation, interstitial deletions or translocations result in the contiguous gene syndrome ATR-16. In this complex syndrome alpha-thalassaemia is accompanied by mental retardation and variable dismorphic features. The study of mutations of the 5' upstream flanking region has led to the discovery of a DNA sequence, localized 40 kb upstream of the zeta-globin gene, which controls the expression of the alpha genes (alpha major regulatory element or HS-40). In the acquired variant of haemoglobin H (HbH) disease found in rare individuals with myelodysplastic disorders and in the X-linked mental retardation associated with alpha-thalassaemia, a profound reduction or absence of alpha gene expression has been observed, which is not accompanied by structural alterations of the coding or controlling regions of the alpha gene complex. Most probably the acquired alpha-thalassaemia is due to the lack of soluble activators (or presence of repressors) which act in trans and affect the expression of the homologous clusters and are coded by genes not (closely) linked to the alpha genes. The ATR-X syndrome results from mutations of the XH2 gene, located on the X chromosome (Xq13.3) and coding for a transacting factor which regulates gene expression. The interaction of the different alpha-thalassaemia determinants results in three phenotypes: the alpha-thalassaemic trait, clinically silent and presenting only limited alterations of haematological parameters, HbH disease, characterized by the development of a haemolytic anaemia of variable degree, and the (lethal) Hb Bart's hydrops fetalis syndrome. The diagnosis of alpha-thalassaemia due to deletions is implemented by the electrophoretic analysis of genomic DNA digested with restriction enzymes and hybridized with specific molecular probes. Recently polymerase chain reaction (PCR) based strategies have replaced the Southern blotting methodology. The straightforward identification of point mutations is carried out by the specific amplification of the alpha 2 or alpha 1 gene by PCR followed by the localization and identification of the mutation with a variety of screening systems (denaturing gradient gel electrophoresis (DGGE), single strand conformation polymorphisms (SSCP)) and direct sequencing.

Animals↗