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[Hemodynamics of the lesser circulation in prolonged hypokinesia (based on data from a morphological study)].

This paper presents data on pulmonary circulation of rats during prolonged hypokinesia (30 to 165 days). It was found that the hypokinetic exposure of 30 to 60 days produced venous and, in particular, capillary plethora associated with blood redistribution and pooling in the lungs. As the exposure continued, the plethora level decreased due to the development of compensatory-adaptive reactions in the lung vessels. For instance, on hypokinetic day 90 small arteries of the muscle type developed a spasm which accelerated circulation stabilization. By hypokinetic days 120-165 pulmonary circulation returned to normal due to the further development of compensatory-adaptive mechanisms in lung vessels (tendency for hypertrophy of the media of small arteries and increase of its cross-sectional area).

Animals↗

PubMed1982

Effects of anemia and hypertransfusion on neonatal marrow and splenic erythrocytic colony-forming units in vitro.

Employing the plasma clot culture system, the effects of anemia or plethora on 10-day-old neonatal rat bone marrow and splenic erythrocytic colony-forming units (CFU-E) were examined. Anemia induced by phenylhydrazine resulted in a decreased CFU-E population in the bone marrow and dramatically increased CFU-E numbers in the spleen. Transfusion-induced plethora increased CFU-E numbers in both the marrow and the spleen. These in vitro findings lend support to studies performed in vivo and further suggest that regulation of erythropoiesis in the neonatal rat differs from that observed in the adult.

Anemia↗

PubMed1981

[Morphology of the circulatory and lymphatic beds of the liver in experimental burns].

Vascular reaction of the liver has been studied in dogs, died and sacrificed during various periods of the burn disease; quantitative characteristics of vascular changes are presented. The data obtained demonstrate that during the whole course of the disease there is a sharp hepatic plethora and sinusoid dilatation demonstrated to a greater extent in the died than in the sacrificed animals. A prolonged capillary congestion (took place in the died animals) is accompanied by more pronounced tissue changes (in comparison with the sacrificed animals) in the form of large foci of albuminous dystrophy and necrotic processes. A suggestion is made that such morphological indices as sharp dilatation of the interlobular arteries and sinuses with pronounced phenomena of plethora, thrombosis of the portal vein branches, large focal hemorrhage could be considered as critical points in adaptation of the peripheral circulation.

Acute Disease↗

PubMed2004

Updates on the treatment of epilepsy in women.

Epilepsy is a condition of the central nervous system that is characterized by recurrent seizures. The goal of management is to make patients seizure free without intolerable adverse effects from treatment. Men and women differ in their physiologic makeup and therefore have different needs that must be considered when attempting to attain this goal. There are special concerns for women of child-bearing years with regard to contraception, pregnancy, and teratogenicity that should be considered during counseling and selection of appropriate treatment. There are also emerging concerns about the interaction of antiepileptic drugs and endocrine function that can affect ovarian function, induce polycystic ovary (PCO)-like syndrome, and threaten fertility. Systemic adverse effects can have a negative impact on weight, cosmetic appearance, sexual function, and bone health. Individualized treatment coupling antiepileptic drug use and the specific phase of impact of the reproductive cycle must be considered in treatment selection. Important concerns regarding long-term therapy are being raised as there are more treatment options to consider because of the plethora of new antiepileptic drugs that are available, often with more favorable pharmacokinetics and different adverse event profiles. Also, sex hormone fluctuations during maturation may exacerbate seizures at particular points during the life cycle for women, including menarche, during menses, during pregnancy, or later in the perimenopausal years, often presenting a uniquely challenging aspect to treatment. As the number of available treatment options for epilepsy increases, the optimal goal for primary care physicians is to work as a team with obstetricians, gynecologists, and neurologists in an effort to ensure the best treatment of women with epilepsy.

Anticonvulsants↗

PubMed1992

Nervous system Lyme borreliosis--revisited [corrected; erratum to be published].

A great deal of confusion surrounds the diagnosis, clinical phenomenology, and treatment of Lyme borreliosis. Most diagnostic methods currently in use are indirect and do not differentiate between prior exposure and current infection. A critical review of the literature permits the characterization of a distinct set of neurologic disorders that are almost certainly caused by this infection and their differentiation from the plethora of syndromes that have been anecdotally linked to infection, but in which causality has never been established. This article describes the range of clinical disorders associated with Lyme borreliosis, provides an overview of current approaches to diagnosis, and reviews current treatment protocols.

Anti-Bacterial Agents↗

PubMed2005

Acute disseminated encephalomyelitis: an update.

Acute disseminated encephalomyelitis (ADEM) is a monophasic autoimmune demyelinating disease of the central nervous system that typically follows a febrile infection or a vaccination. Children are predominantly affected. A plethora of viral and bacterial pathogens and a number of vaccinations have been associated with ADEM. Experimental animal studies indicate that both primary and secondary autoimmune responses contribute to central nervous system inflammation and subsequent demyelination. The clinical diagnosis of ADEM is strongly suggested by a close temporal relationship between an infectious incident or an immunization and the onset of leukoencephalopathic neurological symptoms. Paraclinical tests may support the diagnosis. Particularly helpful are acute signs of newly developed extensive, multifocal, subcortical white matter abnormalities on magnetic resonance images of the brain. The cerebrospinal fluid may disclose a mild lymphocytic pleocytosis and elevated albumin levels. Oligoclonal bands are not always present in ADEM and, if so, may be transient. The major differential diagnosis of ADEM is multiple sclerosis. Treatment options for ADEM consist of anti-inflammatory and immunosuppressive agents. In general, the disease is self-limiting and the prognostic outcome favorable. In the absence of widely accepted clinical or paraclinical diagnostic guidelines, a number of recently conducted observational case series have substantially broadened our understanding about the clinical phenotype, diagnosis, and prognosis of ADEM.

Acute Disease↗

PubMed1999

Users' guides to the medical literature: XVI. How to use a treatment recommendation. Evidence-Based Medicine Working Group and the Cochrane Applicability Methods Working Group.

Clinicians can often find treatment recommendations in traditional narrative reviews and the discussion sections of original articles and meta-analyses. Making a treatment recommendation involves framing a question, identifying management options and outcomes, collecting and summarizing evidence, and applying value judgments or preferences to arrive at an optimal course of action. Each step in this process can be conducted systematically (thus protecting against bias) or unsystematically (leaving the process open to bias). Clinicians faced with a plethora of recommendations may wish to attend to those that are less likely to be biased. Therefore, we propose a hierarchy of rigor of recommendations to guide clinicians when judging the usefulness of particular recommendations. Recommendations with the highest rigor consider all relevant options and outcomes, include a comprehensive collection of the methodologically highest quality data with an explicit strategy for summarizing the data (that is, a systematic review), and make an explicit statement of the values or preferences involved in moving from evidence to action. High rigor recommendations come from systematically developed, evidence-based practice guidelines or rigorously conducted decision analyses. Systematic reviews, which typically do not consider all relevant options and outcomes or make the preferences underlying recommendations explicit, offer intermediate rigor recommendations. Traditional approaches in which the collection and assessment of evidence remains unsystematic, all relevant options and outcomes may not be considered, and values remain implicit, provide recommendations of weak rigor. In an era in which clinicians are barraged by recommendations as to how to manage their patients, this hierarchy provides a potentially useful set of guides.

Decision Making↗

PubMed2005

Why have academic medical centers survived?

Over the past decade, many observers predicted the demise of the academic medical center (AMC) due to competition from community hospitals and physicians, fragile finances, inefficiency, and organizational complexity. In 2004, we interviewed 23 AMC and community hospital administrators to determine why those predictions have proven unfounded, learn the leaders' current concerns and priorities, and to identify desirable changes. Chief concerns were reimbursement uncertainty, federal research policy, ineffective internal decision-making, and clinical quality (mentioned in more than 75% of interviews). Priorities included ensuring sufficient investment capital, revising undergraduate and graduate curricula, strengthening ties with physicians and community hospitals, attracting faculty, and meeting regulatory requirements. We advocate that the AMC: (1) modify the research model to allow greater collaboration with institutions and researchers; (2) enhance free and open export of new and proven clinical techniques and knowledge; (3) devote greater attention to meeting patients' increasing needs for counsel and guidance, not just intervention, given the plethora of complex new technologies and their promotion in the popular media; and (4) simplify their organizations. To accomplish this, it is desirable for future leaders to gain experience outside the AMC, and for faculty and institutions to be less inwardly focused and more attentive to preserving the public's trust.

Academic Medical Centers↗

PubMed1997

Conserved motifs as the basis for recognition of homologous proteins across species boundaries using peptide-mass fingerprinting.

Two-dimensional gel electrophoresis of any biological system presently resolves a plethora of highly purified proteins for which no function or identity has been determined. Theoretical and experimental data were used to demonstrate that peptide-mass fingerprinting (PMF) could aid in the recognition of conserved motifs across species boundaries, and thereby assist in attributing putative function to some of these molecules. Amino acids residue substitutions produced by biological diversity and phylogenetic distance combine to highlight regions of functional significance within proteins. Using 10 prokaryotic and two eukaryotic elongation factors (EF), up to 25 peptide fragments (> 800 Da) per molecule were compared across species boundaries within a 12 x 12 contingency table (66 cross-species comparisons), based upon the degree of molecular mass and amino acid sequence identity. Total amino acid sequence identity ranged from 29.4-80.9% for these molecules. Peptide fragments with homologous sequence across three or more EF were defined as containing, or being near to, conserved functional motifs. Twelve such fragments (> 800 Da) were found in this group of proteins. In addition, an 808.9 Da peptide of unknown functional significance was seen to occur in three of the 12 molecules studied and in another three EF-Tu molecules. At the 83% (five of six residues) identity level, this fragment was found in a further 35 EF-Tu molecules and in 14 unrelated proteins. Further investigation should reveal a role for this fragment (motif) in structural integrity or protein function. A FASTA search conducted on a peptide fragment containing a conserved GTP-binding motif (GHVDHGK) of EF-Tu from Euglena gracilis was used as an example to putatively attribute partial function to three hypothetical proteins derived from DNA sequencing initiatives.

Amino Acid Sequence↗

PubMed1999

The p53 pathway.

Abnormalities of the p53 tumour suppressor gene are among the most frequent molecular events in human and animal neoplasia. Moreover, p53 is one of the most studied proteins in the whole of contemporary biology, with more than 12,500 papers so far written! In this review the choice has been deliberately made not to be fully comprehensive in the coverage of the huge p53 literature. Rather attention is focused on a small number of recent developments which are reviewed in the context of modern models of p53 function. Progress in the analysis of signalling to p53 including phosphorylation cascades, and interactions with proteins such as mdm2 and ARF are highlighted. The plethora of protein-protein interactions is discussed, as are the strategies for defining downstream targets of p53. Finally, the emerging biology of p53 homologues is considered. The need for bridging the gap between reductionist, biochemical and biophysical studies and biological and genetic analysis is emphasized. Only this will provide the needed framework for utilizing the information in clinical care.

Animals↗

PubMed1998

Deconstructing (and reconstructing) cell migration.

An overriding objective in cell biology is to be able to relate properties of particular molecular components to cell behavioral functions and even physiology. In the "traditional" mode of molecular cell biology, this objective has been tackled on a molecule-by-molecule basis, and in the "future" mode sometimes termed "functional genomics," it might be attacked in a high-throughput, parallel manner. Regardless of the manner of approach, the relationship between molecular-level properties and cell-level function is exceedingly difficult to elucidate because of the large number of relevant components involved, their high degree of interconnectedness, and the inescapable fact that they operate as physico-chemical entities-according to the laws of kinetics and mechanics-in space and time within the cell. Cell migration is a prominent representative example of such a cell behavioral function that requires increased understanding for both scientific and technological advance. This article presents a framework, derived from an engineering perspective regarding complex systems, intended to aid in developing improved understanding of how properties of molecular components influence the function of cell migration. That is, cell population migration behavior can be deconstructed as follows: first in terms of a mathematical model comprising cell population parameters (random motility, chemotaxis/haptotaxis, and chemokinesis/haptokinesis coefficients), which in turn depend on characteristics of individual cell paths that can be analyzed in terms of a mathematical model comprising individual cell parameters (translocation speed, directional persistence time, chemotactic/haptotactic index), which in turn depend on cell-level physical processes underlying motility (membrane extension and retraction, cell/substratum adhesion, cell contractile force, front-vs.-rear asymmetry), which in turn depend on molecular-level properties of the plethora of components involved in governance and regulation of these processes. Hence, the influence of any molecular component on cell population migration can be understood by reconstructing these relationships from the molecular level to the physical process level to the individual cell path level to the cell population distribution level. This approach requires combining experimental, theoretical, and computational methodologies from molecular biology, biochemistry, biophysics, and bioengineering.

Cell Count↗

PubMed2000

Innervation of the gastric mucosa.

A plethora of neuronal messengers ("classical" transmitters, gaseous messengers, amino acid transmitters, and neuropeptides) are capable of mediating or modulating gastric functions. Accordingly, the stomach is richly innervated. Gastric nerves are either intrinsic to the gastric wall, i.e., they have their cell bodies in the intramural ganglia and thus belong to the enteric nervous system, or they reach the stomach from outside, originating in the brainstem, in sympathetic ganglia, or in sensory ganglia. Topographically, the nerve fibers in the stomach reach all layers from the most superficial portions of the gastric glands to the outer smooth muscle layer. This wide distribution implies that virtually all different cell types may be reached by neuronal messengers. Within the gastric mucosa endocrine and paracrine cells (e.g., gastrin cells, ECL cells, somatostatin cells), exocrine cells (parietal cells, chief cells, mucous cells), smooth muscle cells, and stromal cells are regulated by neuronal messengers. The sensory innervation, responding to capsaicin, plays an important role in mucosal protection, and in ulcer healing. Presumably also other nerves are involved and a plasticity in the neuropeptide expression has been demonstrated at the margin of gastric ulcers. Taken together, available data indicate a complex interplay between hormones, paracrine messengers and neuronal messengers, growth factors and cytokines in the regulation of gastric mucosal activities such as secretion, local blood flow, growth, and restitution after damage.

Adrenergic Fibers↗

PubMed1997

Analyzing predictive models following definitive radiotherapy for prostate carcinoma.

BACKGROUND: As we approach the 21st century, clinically useful predictive models for prostate carcinoma are urgently needed to stratify patients reliably for future treatment strategies. Recently, many investigators have developed models that employ prostate specific antigen (PSA)-based constructs or groupings in an attempt to predict outcome accurately following definitive radiotherapy. This investigation was conducted to determine which of these models provides the closest "fit" to independent clinical outcome data measuring biochemical freedom from failure (bNED control), thereby warranting further exploration. METHODS: Six models were analyzed in a definitive radiotherapy series of 421 patients with localized prostate carcinoma treated with a median dose of 74 Gray (Gy) between March 1988 and November 1994. A stepwise Cox proportional hazards multivariate analysis (MVA) was performed to predict for bNED control using the following covariates: PSA, Gleason's score, stage, dose, PSA density, and perineural invasion. Subsequent MVAs were performed for each model incorporating the new construct or prognostic groupings. The adequacy of the models was confirmed using plots of score residuals against time to bNED failure and comparisons were made used Akaike's Information Criteria (AIC) in which a smaller value corresponds to a statistically improved model based on explained variation and the number of predictors. Because PSA was distributed in a log-normal fashion in the current study population, the model-building process was duplicated using a logarithmic transformation analysis. Biochemical failure was defined as 2 consecutive elevations in the PSA > or = 1.5 ng/mL. The median follow-up time was 34 months (range, 2-87 months). RESULTS: Initially, the model developed by Pisansky et al. appeared the most predictive due to the parsimony in their risk estimate, which is the sole predictor of outcome, as well as its associated lowest AIC value. However, after the logarithmic transformation analysis, all the models appeared to be equally predictive of bNED outcome. CONCLUSIONS: A plethora of accurate models for predicting outcome following definitive radiotherapy for prostate carcinoma recently have been engineered, all of which are essentially equally predictive in this data base (via a logarithmic conversion process). This analysis should be corroborated in other large radiotherapy series.

Follow-Up Studies↗

PubMed2000

Predominance of brain tumors in an extended Li-Fraumeni (SBLA) kindred, including a case of Sturge-Weber syndrome.

BACKGROUND: Li-Fraumeni syndrome (LFS) is characterized by a plethora of cancers, most prominent of which is carcinoma of the breast followed by sarcomas, brain tumors, leukemia, lymphoma, lung carcinoma, and adrenocortical carcinoma (therefore, also referred to by the acronym SBLA syndrome). METHODS: The family reported herein was first described 2 decades ago. Now extensive follow-up has shown the predictable occurrence of these tumor types, in addition to an excess of brain tumors and the finding of Sturge-Weber syndrome (SWS) in an LFS-affected family member. RESULTS: A possible new feature of the disorder, suggestive of SWS, was identified in a patient in the direct genetic lineage. This patient had a rhabdomyosarcoma of the eyelid at age 29 months and at age 14 years was diagnosed with lymphoblastic lymphoma/acute lymphoblastic leukemia. A remarkable excess of brain tumors was identified in this family through this current update. The p53 germ-line mutation was not identified in any affected member of this family. CONCLUSIONS: To the authors' knowledge, this is the first example of SWS in the context of LFS. Brain tumors appear to be an important component of the tumor spectrum of LFS, as evidenced in this family.

Adult↗

PubMed1999

Expression of transforming-growth-factor (TGF)-beta receptors and Smad proteins in glioblastoma cell lines with distinct responses to TGF-beta1.

A panel of 6 human glioma cell lines was examined for TGF-beta1 responsiveness. U-178 MG and U-251 MG AgCl1 were significantly inhibited by TGF-beta1, while U-343 MGa 31L and U-343 MGa 35L were potently stimulated to proliferate. TGF-beta1 induced endogenous PAI-1 protein synthesis, Smad binding element/(CAGA)12-luciferase-reporter activity, as well as mRNA expression of Smad6 and Smad7 in all gliomas. Interestingly, TGF-beta1 differentially stimulated or inhibited the expression of TbetaR-I and TbetaR-II mRNA in the gliomas. Affinity cross-linking studies using 125I-TGF-beta1 revealed that the gliomas expressed TGF-beta-type-I(TbetaR-I) and -type-II(TbetaR-II) receptors, although binding to TbetaR-II in U-343 MGa 31L and U-251 MG AgCl1 was low to undetectable. Smad2 protein was abundantly present in U-178 MG, U-343 MG, and U-343 MGa 35L, while Smad3 was readily detectable in U-178 MG, U-343 MG, U-343 MGa 35L and U-251 MG AgCl1. In all gliomas, TGF-beta1 induced phosphorylation of Smad2. The level to which TGF-beta1 could activate the pathway leading to induction of the (CAGA)12-luciferase reporter seemed to correlate to the expression levels of TGF-beta receptors, Smad3 and Smad4 proteins. However, despite the plethora of data regarding TGF-beta1 signalling in the different glioma cell lines, the mechanism underlying the differential growth effects mediated by TGF-beta1 is still unclear. The results suggest that a complex balance between several components in the TGF-beta signalling pathway controls glioma responsiveness to TGF-beta1, and extend reports indicating that distinct signal transduction pathways are involved in growth inhibition and other cellular responses.

DNA, Neoplasm↗

PubMed1999

Highly basic myelin and oligodendrocyte proteins analyzed by NEPHGE-two-dimensional gel electrophoresis: recognition of novel developmentally regulated proteins.

Two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) provides high resolution separation of proteins and offers a powerful method for their identification and characterization. Since many myelin-specific proteins are highly basic, they cannot readily be analyzed by standard isoelectric focusing (IEF)-2D-PAGE that affords separation primarily in the isoelectric points (pI) range of 4-8. An alternative method, nonequilibrium pH gradient electrophoresis (NEPHGE)-2D-PAGE, can provide excellent resolution of highly basic proteins. In the present study, we have optimized the NEPHGE-2D-PAGE protocol for the analysis of myelin proteins with basic pIs, and provide a NEPHGE-2D-PAGE map based on size, pI, and immunoreactivity (Western blot) of myelin basic protein (MBP), 2', 3'-cyclic-nucleotide 3'-phosphodiesterase (CNP), myelin proteolipid protein (PLP), and its smaller spliced variant DM20, myelin/oligodendrocyte glycoprotein (MOG) and oligodendrocyte-specific protein (OSP). We have also demonstrated, by analyzing metabolically radiolabeled oligodendrocytes in culture at specific stages of the developmental lineage, the developmentally up-regulated expressions of several undefined, oligodendrocyte, basic membrane proteins during oligodendrocyte differentiation. We suggest that this approach offers an important tool for identifying and characterizing the plethora of uncharacterized myelin proteins.

Animals↗

PubMed1997

Selection for genome instability by DNA damage in human cells: unstable microsatellites and their consequences for tumourigenesis.

The emergence of tumour cells resistant to chemotherapeutic treatment is a major confounding factor in anticancer treatment. Many chemotherapeutic drugs are DNA damaging agents. Resistance to DNA damage can be acquired via a plethora of different mechanisms, including, surprisingly, loss of DNA mismatch repair activity. The DNA mismatch repair system acts after DNA replication and corrects non-Watson-Crick base pairs and other replication errors. Human cells lacking mismatch repair activity have high spontaneous mutation rates. Frequent frameshift mutations in repetitive DNA sequences are characteristically associated with the defect. This hypermutability at repetitive sequences is termed microsatellite instability. DNA mismatch repair defects underlie a predisposition to cancer and are associated with a significant fraction of apparently sporadic cancer cases. In contrast to many other neoplasms, gross genetic aberrations are rare in cells from tumours with microsatellite instability. In these mismatch repair-defective tumours, certain genes that would normally hinder tumour development are frequently found to be inactivated by frameshift mutations in repetitive DNA tracts within their coding sequences. This implies that the small-scale genome alterations characteristic of mismatch repair defects can act as a driving force in tumour development.

Antineoplastic Agents↗

PubMed1999

Guanosine-rich oligodeoxynucleotides induce proliferation of macrophage progenitors in cultures of murine bone marrow cells.

Widely used to specifically inhibit gene expression, synthetic oligodeoxynucleotides (ODN) can exert a plethora of non-antisense effects. Immunostimulation by CpG-ODN has attracted particular attention. ODN rich in the nucleotide guanosine (G-rich ODN) constitute another type of sequences displaying non-antisense-mediated effects. We have examined the effects of CpG- and G-rich ODN on primary mouse bone marrow cells (BMC) in vitro. CpG-ODN induced rapid proliferation of B cells and production of IL-6 and IL-12p40. However, when tested in agar colony assays, CpG-ODN failed to promote the formation of colonies. In marked contrast, G-rich non-CpG-ODN led to sustained proliferation of macrophage-like cells without inducing cytokines or hemopoietic growth factors. Unlike CpG-ODN, G-rich ODN effectively induced the formation of macrophage colonies in agar assays, indicating a direct action on progenitor cells. Electrophoretic mobility shift assays revealed specific binding of G-rich ODN to a non-nuclear protein. The ability of a panel of ODN to compete for binding correlated with their potential to induce proliferation of macrophage-like cells from primary mouse BMC. As such, these data reveal a so far unrecognized potential of G-rich ODN to signal directly outgrowth of macrophage progenitors from BMC.

Agar↗