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PubMed2002

Early intervention with immunomodulatory agents in the treatment of multiple sclerosis.

Multiple sclerosis (MS) is a lifelong neurologic disease leading to moderate or severe disability in the majority of affected patients. Studies of the natural history of MS suggest that 90% of patients with relapsing-remitting MS eventually develop secondary progressive (SP) disease. Magnetic resonance imaging (MRI) studies have consistently shown a high frequency of new T2 lesions and new gadolinium enhancing lesions even in the absence of clinical relapse. Lesion burden on T2 MRI increases by 5% to 10% per year and both axonal transection and cerebral atrophy are present at the earliest stages of RR MS. A wealth of evidence suggests that MS is a disease process that is continuously active, and that irreversible damage occurs early in the disease. Despite knowledge of the natural history and the availability of treatments that reduce relapse rates, decrease the accumulation of disability, and decrease surrogate measures of disease activity, only 60% of eligible patients have been treated with immunomodulating agents. This paper reviews the available evidence suggesting that immunomodulatory therapy modifies the natural history of MS and presents an argument for early intervention in the treatment of MS.

Adjuvants, Immunologic↗
PubMed2007

Biomass allocation is an important determinant of the tannin concentration in growing plants.

BACKGROUND AND AIMS: Condensed tannins (CTs) in the diet affect consumers in a concentration-dependent manner. Because of their importance in plant defence against herbivores and pathogens as well as their potential application against gastrointestinal parasites of ruminants in agronomy, an understanding of the seasonal dynamics of CT concentrations during plant growth is essential. METHODS: Over a vegetation period, CT concentrations in leaves, stems and roots and the biomass proportions between these organs were investigated in Onobrychis viciifolia, Lotus corniculatus and Cichorium intybus. Based on the experimental data, a model has been suggested to predict CT concentrations in harvestable biomass of these species. KEY RESULTS: During the experiment, leaf mass fractions of plants decreased from 85, 64, 85 to 30, 18, 39 % d. wt in Onobrychis, Lotus and Cichorium, respectively, and proportions of stems and roots increased accordingly. While CT concentrations almost doubled in leaves in Onobrychis (from 52 to 86 mg g(-1) d. wt, P<0.001) and Lotus (from 25 to 54 mg g(-1) d. wt, P<0.001), they were stable at low levels in expanding leaves of Cichorium (5 mg g(-1) d. wt) and in stems and roots of all investigated species. Due to an inverse effect of the increasing CT concentrations in leaves and simultaneous dilution from increasing proportions of 'CT-poor' stems, CT concentrations in harvestable biomass were stable over time in all investigated species: 62, 26 and 5 mg g(-1) d. wt for Onobrychis, Lotus and Cichorium, respectively. CONCLUSIONS: As a consequence of the unequal distribution of tannins in different plant parts and due to the changing biomass proportions between them, various herbivores (e.g. a leaf-eating insect and a grazing ruminant) may find not only different concentrations of CT in their diets but also different CT dynamics during the season. For the prediction of seasonal variations of CT concentrations, biomass allocation and accumulation of none-CT plant material are likely to be as important predictors as the knowledge of CT synthesis and its regulation.

Biomass↗
PubMed2005

Structural assessment of the urethral sphincter in women with urinary retention.

PURPOSE: The pathophysiology of urinary retention in women is generally unknown but a subgroup of women with urinary retention have been diagnosed as having so-called primary disorder of sphincter relaxation on the basis of an abnormal urethral sphincter electromyogram. It was suggested this sphincter overactivity could lead to work hypertrophy of the urethral rhabdosphincter and in this study we looked for any evidence of such muscle fiber hypertrophy. MATERIALS AND METHODS: In 9 women 18 to 45 years old (mean age 31.6) with urinary retention and overactive urethral sphincter electromyogram, light and electron microscopy were used to examine core needle biopsies of the urethral rhabdosphincter taken under transvaginal ultrasound control. Of the 9 patients only 5 biopsies processed for light microscopy and 4 processed for electron microscopy contained striated urethral muscle fibers. The results of these biopsies were compared to the morphology of a control specimen from a postmenopausal woman without a history of urinary retention. RESULTS: On light microscopy the urethral rhabdosphincter fiber diameter did not differ among patients (mean average 7.6 mum), was less than that reported in the literature (15 to 20), but did not differ from that of the control (mean 9.9). In all patients electron microscopy showed excessive peripheral sarcoplasm with lipid and glycogen deposition, and sarcoplasmic accumulation of normal mitochondria. These ultrastructural abnormalities were not seen in the control. CONCLUSIONS: To our knowledge this is the first morphological description of the urethral rhabdosphincter in a subgroup of women with urinary retention. Mean rhabdosphincter fiber diameter was approximately the same in patients and controls. This study does not support the previous theory that urethral sphincter overactivity in a subgroup of women with urinary retention leads to work hyperplasia of urethral rhabdosphincter fibers. An alternative hypothesis is suggested.

Adolescent↗
PubMed2000

Statistical methods for the objective design of screening procedures for macromolecular crystallization.

The crystallization of a new macromolecule is still very much a trial-and-error process. As is well known, it requires the search of a large parameter space of experimental settings to find the relatively few idiosyncratic conditions that lead to diffraction-quality crystals. Crystallographers have developed a variety of screens to help identify initial crystallization conditions, including those based on systematic grids, incomplete factorial and sparse-matrix approaches. These are somewhat subjectively formulated based on accumulated data from past crystallization experiments. Ideally, one would prefer as objective a procedure as possible; however, that requires objective methods that incorporate a broad source of crystallization data. The Biological Macromolecular Crystallization Database (BMCD), a repository of all published crystallization conditions, is an obvious source of this data. This database has been augmented with a hierarchical classification of the macromolecules contained in the BMCD as well as extensive data on the additives used with them. A statistical analysis of the augmented BMCD shows the existence of significant correlations between families of macromolecules and the experimental conditions under which they crystallize. This in turn leads to a Bayesian technique for determining the probability of success of a set of experimental conditions based on the data in the BMCD as well as facts about a macromolecule known prior to crystallization. This has been incorporated into software that enables users to rank experimental conditions for new macromolecules generated by a dense partial factorial design. Finally, an additional advantage of the software described here is that it also facilitates the accumulation of the data required for improving the accuracy of estimation of the probabilities of success - knowledge of the conditions which lead to failure of crystallization.

Crystallization↗
PubMed2000

Towards an understanding of equine pleuropneumonia: factors relevant for control.

OBJECTIVE: To review relevant literature on factors associated with the development of equine pleuropneumonia. DESIGN: A review of the literature using a range of databases including Current Contents, Medline, ChemAbstracts, Biological Abstracts and CAB and a comprehensive search strategy which involved use of keywords, author and subject category searches. Additional sources included review of articles cited by key accumulated references. RESULTS: Since the early years of this century, many of the "gaps" in our knowledge of the pathogenesis of this disease have been filled. We now know that equine pleuropneumonia results from contamination of the lower respiratory tract with bacteria similar to the normal oropharyngeal microbiota of the horse and that transportation of any mode, especially over long distances (and consequently with no or short rest periods), is the single most important predisposing factor for this disease. This is associated with restraint of horses such that they are unable to lower their heads, which leads to increased opportunity for lower respiratory tract contamination and a reduced opportunity for clearance. Strenuous exercise also results in lower respiratory tract contamination and exercise subsequent to transportation exerts additive detrimental effects on the defenses of the lower respiratory tract. CLINICAL IMPLICATIONS: While modern veterinary medicine and surgery have significantly reduced the death rate from pleuropneumonia, horses that develop the disease have a high probability of not returning to their prior use. This underscores the importance of developing the most effective strategies for its prevention.

Animals↗
PubMed2005

Intermediate care: for better or worse? Process evaluation of an intermediate care model between a university hospital and a residential home.

BACKGROUND: Intermediate care was developed in order to bridge acute, primary and social care, primarily for elderly persons with complex care needs. Such bridging initiatives are intended to reduce hospital stays and improve continuity of care. Although many models assume positive effects, it is often ambiguous what the benefits are and whether they can be transferred to other settings. This is due to the heterogeneity of intermediate care models and the variety of collaborating partners that set up such models. Quantitative evaluation captures only a limited series of generic structure, process and outcome parameters. More detailed information is needed to assess the dynamics of intermediate care delivery, and to find ways to improve the quality of care. Against this background, the functioning of a low intensity early discharge model of intermediate care set up in a residential home for patients released from an Amsterdam university hospital has been evaluated. The aim of this study was to produce knowledge for management to improve quality of care, and to provide more generalisable insights into the accumulated impact of such a model. METHODS: A process evaluation was carried out using quantitative and qualitative methods. Registration forms and patient questionnaires were used to quantify the patient population in the model. Statistical analysis encompassed T-tests and chi-squared test to assess significance. Semi-structured interviews were conducted with 21 staff members representing all disciplines working with the model. Interviews were transcribed and analysed using both 'open' and 'framework' approaches. RESULTS: Despite high expectations, there were significant problems. A heterogeneous patient population, a relatively unqualified staff and cultural differences between both collaborating partners impeded implementation and had an impact on the functioning of the model. CONCLUSION: We concluded that setting up a low intensity early discharge model of intermediate care between a university hospital and a residential home is less straightforward than was originally perceived by management, and that quality of care needs careful monitoring to ensure the change is for the better.

Aged↗
PubMed2005

Distribution of Cryptosporidium parvum sporozoite apical organelles during attachment to and internalization by cultured biliary epithelial cells.

Although accumulating evidence supports an active role for host cells during Cryptosporidium parvum invasion of epithelia, our knowledge of the underlying parasite-specific processes triggering such events is limited. In an effort to better understand the invasion strategy of C. parvum, we characterized the presence and distribution of the apical organelles (micronemes, dense granules, and rhoptry) through the stages of attachment to, and internalization by, human biliary epithelia, using serial-section electron microscopy. Novel findings include an apparent organized rearrangement of micronemes upon host cell attachment. The apically segregated micronemes were apposed to a central microtubule-like filamentous structure, and the more distal micronemes localized to the periphery and apical region of the parasite during internalization, coinciding with the formation of the anterior vacuole. The morphological observations presented here extend our understanding of parasite-specific processes that occur during attachment to, and internalization by, host epithelial cells.

Animals↗
PubMed1998

Lessons from gene knockouts.

The authors describe the technique for the application of homologous recombination in embryonic stem cells, which is now widely used to engineer mice which carry specific knockouts of genes. A summary is given of some of the knowledge of the pathogenesis of and resistance to infections with parasites, bacteria, or viruses which has accumulated during recent years, based on the investigation of knockout mice. Special emphasis is placed on knockout animals which lack components of the cytokine network, lack genes which are critical for the correct presentation of antigens or are deficient in different immune cell subsets. In addition, a brief explanation is offered of the possibilities for inducing targeted deletions or mutations in genes of livestock species (e.g., by nuclear transfer or by mutagenesis using the alkylating agent N-ethyl-N-nitrosourea) which could lead to the breeding of animals which are resistant to infectious diseases in the future.

Animals↗
PubMed2001

Molecular biology of pancreatic cancer: potential clinical implications.

The development of cancer involves the accumulation of genetic changes. Over the past decade there has a been spectacular advance in the knowledge of the genetic basis of cancer, mainly as a result of the rapid progression of molecular technology. Pancreatic cancer is one of the most lethal cancers. Conventional therapeutic approaches have not had much impact on the course of this aggressive neoplasm. Knowledge of the molecular biology of pancreatic cancer has grown rapidly. Genetic alterations in pancreatic cancer include oncogene mutations (most commonly K-ras mutations), and tumour suppressor gene alterations (mainly p53, p16, DCC, etc.). These advances have potential implications for the management of this deadly disease. Identification of a hereditary genetic predisposition to pancreatic cancer has led to the formation of pancreatic cancer registries around the world, with voluntary screening of patients and siblings for the hereditary genetic defect. Asymptomatic population screening remains unrealistic, but the recognition of subpopulations at increased risk from pancreatic cancer, along with novel and sensitive detection techniques, means that targeted population screening is a step closer. Intensive research is performed in specialist laboratories to improve the diagnostic approach in patients with pancreatic cancer. The use of such molecular diagnostic methods is likely to expand. Molecular biology may also have a great impact on the treatment of pancreatic cancer, and many therapeutic approaches are being evaluated in clinical trials, including gene replacement therapy, genetic prodrug activation therapy, antisense immunology and peptide technology. The 'molecular age' has the promise of delivering still better results. This review summarises recent data relating to the molecular biology of pancreatic cancer, with emphasis on features that may be of clinical significance for diagnosis and/or therapy.

Genes, Tumor Suppressor↗
PubMed1995

Kinetic modelling of in vitro lipid peroxidation experiments--'low level' validation of a model of in vivo lipid peroxidation.

Kinetic modelling overcomes some of the drawbacks of purely intuitive thinking in integrating information accumulated on chemical reactions involved in oxidative stress. However, it is important to assess if current knowledge about the reactions that mediate lipid peroxidation already allows satisfactory modelling of this process in near-to-physiological conditions. In this paper, a set of increasingly complex in vitro experiments on antioxidants (alpha-tocopherol and ascorbate) and lipid peroxidation in heterogeneous systems is simulated. Quantitative to semiquantitative agreement is found between experimental and simulation results. In addition, this theoretical analysis provided useful insights, suggested new hypotheses and experiments and pointed out relevant aspects needing further research. The results encourage and serve as partial validation for the formulation of relatively detailed mathematical models of in vivo lipid peroxidation. Some important aspects of the formulation and analysis of such models are discussed.

Antioxidants↗
PubMed1999

Can oxypurines plasma levels classify the type of physical exercise?

BACKGROUND: A laboratory-based model able to describe muscle energy status during physical exercise and changes in myofibrillar composition in response to training would be desirable. Lactate and ammonia concentrations are not sufficient for a comprehensive knowledge of these systems. All muscle fibres, irrespective of the type, show ATP depletion and IMP accumulation following exhausting muscular exercise with quantitative differences due to the different concentrations of deaminase. We studied the plasma concentration of metabolites of oxypurine cascade to test their reliability to classify different exercises. METHODS: We studied 52 athletes, measuring plasma metabolites at the beginning and at the end of their specific field exercise (cycle pursuers, 8 cases; soccer players, 19; marathon runners, 25). K3EDTA-blood samples were assayed for plasma hypoxanthine, xanthine, and inosine, using an HPLC technique, as well as ammonia and lactate by means of enzymatic methods. RESULTS AND CONCLUSIONS: Basal oxypurines levels were not different in relation to any specific physical exercise. Post-exercise oxypurines, namely hypoxanthine, were more precise predictors of muscle energy exhaustion than strain intensity or duration. Plasma levels of hypoxanthine may be elevated also in the presence of normal xanthine and uric acid concentrations, due to an exhaustion of the enzymatic pathway, to a reduced activity of xanthine-oxidase or finally to a substrate-dependent inhibition of the process.

Ammonia↗
PubMed2002

Genetic epidemiology of juvenile idiopathic arthritis.

Juvenile idiopathic arthritis (JIA) is a heterogeneous group of disorders. Although the pathogenesis is not completely understood, many studies point to a genetic component in the susceptibility for this disease with environmental factors also contributing to the pathogenesis. The genetic component of JIA is complex, involving the effects of multiple genes at various points in the disease pathology. The best documented association is with the genes within the Human Leukocyte Antigen (HLA) complex, encoding the classical peptide-presenting molecules. JIA is associated with particular alleles at, at least, three different HLA loci: HLA-A (HLA-A*0201), -DR/DQ (DRB1*08, DRB1*11, DRB1*13) and -DP (DPB1*0201, DPB1*0301), with marked differences between the disease subtypes. Non-HLA genes may also contribute to the disease. Many of these genes encode cytokines and probably regulate their production. Examples of such cytokines involved in JIA are interleukin-1 alpha (IL-1 alpha), interleukin-1 receptor antagonist (IL-1Ra), interleukin-6 (IL-6), interleukin-10 (IL-10), macrophage inhibitory factor (MIF), interferon regulatory transcription factor (IFN1). Accumulated data suggest that interactions between the genes are necessary for the development of the disease. Knowledge of the genes involved would help to understand the molecular mechanisms involved in the pathogenesis of JIA and may have implications for prognosis and therapy.

Adolescent↗
PubMed1986

Total parenteral nutrition during pregnancy.

Parenteral hyperalimentation or total parenteral nutrition has become an established therapy for patients with a wide variety of conditions that preclude oral feeding. Because pregnancy is an infrequent event in poorly nourished women with acute or chronic illness, total parenteral nutrition has not been widely used for pregnant patients. Some obstetricians believe that total parenteral nutrition entails risks in excess of its potential benefit to pregnancy and demands skills and knowledge that are either not available or are in limited supply. Sufficient favorable clinical experience has accumulated over the past 15 years so that total parenteral nutrition can be recommended in the management of malnutrition during pregnancy. The purpose of this report is to review the authors' experience and the literature about total parenteral nutrition during pregnancy.

Adult↗
PubMedDate not supplied

Renal amyloidosis in childhood. An overview of the topic with 25 years experience.

Amyloidosis is a heterogeneous group of diseases characterized by extracellular accumulation of an eosinophilic, hyalin and proteinaceous material containing mucopolysaccharide substance in various tissues and organs. Knowledge about the chemical structure of amyloid fibril proteins has led to the recognition of various forms of amyloidosis including Amyloid-A (AA), Amyloid-L (AL), hereditary, senile, dialysis-related, localized and cerebral amyloidosis. It is now recognized that all types of amyloid contain amyloid P (AP) component which is derived from the serum amyloid P component, a normal circulating glycoprotein and a member of the pentraxin family. A recent classification proposed by WHO-IUIS (Nomenciature Subcommittee) is based on the chemical nature of amyloid fibris rather than their clinical and pathologic features. The kidneys are frequently involved, and renal failure is the major cause of death. Childhood renal amyloidosis is almost always secondary (reactive, AA type) and usually associated with chronic inflammatory, infectious and heredofamilial diseases. In developed countries, rheumatoid arthritis is the most common cause of renal amyloidosis, while in developing countries patients with familial Mediterranean fever (FMF) (untreated) and chronic suppurative infections constitute a large proportion of renal amyloidosis cases. No specific therapy is currently available for amyloidosis. Once renal amyloidosis develops, progress to end-stage renal failure is almost inevitable within 2-13 years. The aim of treatment is to give effective supportive therapy and to control the underlying diseases by colchicine, alkylating agents and appropriate antibiotics. The prognosis of patients with end-stage renal failure can be improved by maintenance dialysis and renal transplantation. The growing knowledge about the pathogenesis and chemical nature of amyloid fibris may open up further avenues for the discovery of specific therapeutic modalities against amyloidosis.

Adolescent↗
PubMed2001

Role of S6 phosphorylation and S6 kinase in cell growth.

This article reviews our current knowledge of the role of ribosomal protein S6 phosphorylation and the S6 kinase (S6K) signaling pathway in the regulation of cell growth and proliferation. Although 40S ribosomal protein S6 phosphorylation was first described 25 years ago, it only recently has been implicated in the translational up-regulation of mRNAs coding for the components of protein synthetic apparatus. These mRNAs contain an oligopyrimidine tract at their 5' transcriptional start site, termed a 5'TOP, which has been shown to be essential for their regulation at the translational level. In parallel, a great deal of information has accumulated concerning the identification of the signaling pathway and the regulatory phosphorylation sites involved in controlling S6K activation. Despite this knowledge we are only beginning to identify the direct upstream elements involved in growth factor-induced kinase activation. Use of the immunosupressant rapamycin, a bacterial macrolide, in conjunction with dominant interfering and activated forms of S6K1 has helped to establish the role of this signaling cascade in the regulation of growth and proliferation. In addition, current studies employing the mouse as well as Drosophila melanogaster have provided new insights into physiological function of S6K in the animal. Deletion of the S6K1 gene in mouse cells led to an animal of reduced size and the identification of the S6K1 homolog, S6K2, whereas loss of dS6K function in Drosophila demonstrated its paramount importance in development and growth control.

Amino Acid Sequence↗
PubMed2003

FDG-PET for evaluating musculoskeletal tumors: a review.

Positron-emission tomography (PET) can provide an in vivo method for evaluating metabolism and physiology in normal and diseased tissues. Clinical trials with [(18)F]2-deoxy-2-fluoro- d-glucose (FDG), the most commonly used radiolabeled tracer for PET imaging, have demonstrated increased accumulation of FDG in several cancer tissues. In this article, we introduce the basic principles of FDG-PET and review current knowledge about FDG-PET for evaluating musculoskeletal tumors. Recent reports and our own experience suggest that FDG-PET cannot be a screening method for differential diagnosis between benign and malignant musculoskeletal lesions, including many neoplasms originating from different tissues altogether. FDG-PET might not accurately reflect the malignant potential of musculoskeletal tumors, but rather might implicate cellular components included in the lesions. A high accumulation of FDG can be observed in histiocytic, fibroblastic, and some neurogenic lesions, regardless of whether they are benign or malignant. More specific uses of FDG-PET, such as grading, staging, and monitoring of musculoskeletal sarcomas, should be considered for each tumor of a different histologic subtype.

Bone Neoplasms↗
PubMed1984

An immediate increase in calcium accumulation by rat thymocytes induced by triiodothyronine: its role in the subsequent metabolic responses.

In previous studies we have shown that the thyroid hormone T3 induces a prompt increase in the cAMP concentration of rat thymocytes in vitro. This is followed by and very likely leads to an increase in cellular uptake of the glucose analog 2-deoxyglucose (2-DG). Since these effects of T3 were shown to require the presence of Ca2+ in the suspending medium, it seemed reasonable to determine whether T3 would influence the metabolism of calcium itself. In standard medium containing 1 mM Ca2+ and 45Ca as a tracer, T3 induced a very prompt, dose-related, but transient, increase in thymocyte calcium accumulation. This effect was evident within the first minute after the addition of T3 (including processing time) and is to our knowledge the most rapid effect of T3 yet demonstrated. The effect reached a maximum very shortly thereafter and then abated within a few minutes. Uptake of 45Ca from Ca2+-free medium (5 microM Ca2+ as a contaminant) was also increased by T3, but under these conditions, the increase was sustained for the entire 120-min period of study. At a concentration of 25 microM, lanthanum (La3+) unexpectedly produced a rapid and marked (4- to 6-fold) increase in 45Ca accumulation in the thymocytes. The increase in cellular calcium accumulation produced by La3+ was not associated with any effect on thymocyte cAMP concentration or 2-deoxyglucose (2-DG) uptake. However, La3+ potentiated the response of the cell to T3 in respect to calcium accumulation, cAMP concentration, and 2-DG uptake, shifting the dose-response curve of the latter two effects to the left. In view of the calcium dependence of the T3 effect on thymocyte cAMP concentration and 2-DG uptake, and the effect of La3+ to concomitantly enhance the sensitivity of the cell to the effects of T3 on calcium accumulation and cAMP and 2-DG metabolism, we suggest that the prompt increase in cellular Ca2+ uptake induced by T3 that we demonstrated is causally related to its subsequent effect on cellular cAMP concentration and 2-DG uptake.

Animals↗
PubMed1992

T-lymphocytes that accumulate in the lung in sarcoidosis have evidence of recent stimulation of the T-cell antigen receptor.

Sarcoidosis, a granulomatous disease of unknown etiology, is characterized at sites of disease such as the lung by the accumulation of large numbers of T-lymphocytes. To differentiate whether the T-cells accumulate in organs nonspecifically (e.g., through chemotaxis or tumorlike proliferation) or more specifically through an antigen-driven ordered immune response, the present study capitalized on the knowledge that specific antigen stimulation of T-cells requires antigen interactions with the T-cell antigen receptor (TCR), resulting in a decrease in the number of surface TCR and a concomitant increase in TCR mRNA levels, i.e., if lung T-cell accumulation in pulmonary sarcoid results from an ordered immune response, lung, but not blood, T-cells should demonstrate evidence of recent triggering of the alpha beta receptor, the most abundant type of TCR. The surface density of T-cell surface alpha beta TCR expression was evaluated by flow cytometry with an anti-alpha beta antibody and TCR beta-chain mRNA transcript number quantified by in situ hybridization with 35S-labeled antisense and sense cRNA probes. Control studies utilizing normal blood T-lymphocytes stimulated with the anti-CD3 monoclonal antibody, OKT3, in the presence of autologous monocytes, demonstrated the expected down-regulation of surface alpha beta TCR expression and increased beta-chain mRNA transcript number. When lung and blood T-cells of patients with pulmonary sarcoidosis were compared immediately upon recovery (i.e., without in vitro stimulation), the lung T-cells of 10 of 10 subjects demonstrated a decreased surface density of alpha beta TCR compared with their autologous blood T-cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗