bluuebunny/crossref_metadata_2025_split huggingface dataset:
Carcinoid metastasis to the brain
Authors: Hlatky Roman , Suki Dima , Sawaya Raymond 
Published: October 2004

AbstractBACKGROUNDCarcinoid tumors rarely metastasize to the brain. The objectives of the current study were to assess the frequency of brain metastasis from carcinoid tumors, determine correlates of survival, and describe treatment modalities and their outcomes.METHODSBetween January 1977 and December 2003, 1633 patients with a carcinoid tumor were registered at The University of Texas M. D. Anderson Cancer Center. Of those, 24 patients (1.5%) had a diagnosis of brain metastasis. The authors collected demographic and clinical data and performed a statistical analysis.RESULTSThe median age at the time patients were diagnosed with brain metastasis was 60 years. The metastases were treated with whole‐brain radiotherapy (WBRT) alone in 7 patients (29%), and 12 patients (50%) underwent surgical resection, 7 of whom (29%) also received WBRT. The median survival time for the entire cohort after diagnosis of the primary tumor was 2.3 years (95% confidence interval [CI], 0.5–4.1 years), and the median survival time after the diagnosis of brain metastasis was 10.0 months (95% CI, 4.0–16.0 months). The longest median survival observed after the diagnosis of brain metastasis (3.2 years) occurred in patients who underwent resection and received WBRT. In the multivariate analysis, the adjusted rate ratio for comparison of all treatments versus combination of neurosurgical intervention and WBRT was 5.7 (95% CI, 1.3–26.1;P= 0.024). A positive effect of surgery followed by WBRT on the duration of survival was detected in patients with a single metastasis (P= 0.084) as well as in those with multiple metastases (P= 0.018).CONCLUSIONSProlonged survival was observed in patients < 65 years old as well as in those who underwent surgery and received WBRT in comparison with other treatments. Whenever feasible, neurosurgical resection followed by WBRT seems to be the indicated treatment in patients with brain metastases from carcinoid tumors. Cancer 2004. © 2004 American Cancer Society.
Inverse association between prostatic polyunsaturated fatty acid and risk of locally advanced prostate carcinoma
Authors: Freeman Vincent L. , Meydani Mohsen , Hur Kwan , Flanigan Robert C. 
Published: October 2004

AbstractBACKGROUNDAn effect of fatty acids has been implicated in men with advanced‐stage prostate carcinoma and in men who have died of the disease. To evaluate the influence of fatty acids in men with prostate carcinoma at earlier stages, the authors examined the relation between prostatic concentrations of fatty acids and locally advanced prostate carcinoma in men with clinically organ‐confined disease.METHODSFatty acids were measured by capillary gas chromatography in fresh, nonmalignant prostate tissue specimens collected during surgery from 196 men undergoing radical prostatectomy for localized prostate carcinoma. Two‐sided, two‐sample Student t tests compared mean concentrations in men with extraprostatic disease (pT3–4N0–1M0) with control men with organ‐confined disease. Logistic regression accounted for clinical stage, prostate‐specific antigen level, Gleason sum, and other factors.RESULTSPercent total prostatic polyunsaturated fatty acid (PUFA) was found to be inversely associated with risk of locally advanced prostate carcinoma (n = 52) (odds ratio [OR] = 0.93, 95% confidence interval [95% CI], 0.87–0.99; P = 0.035). Risk of seminal vesicle involvement accounted for this association (OR = 0.86, 95% CI, 0.78–0.95; P = 0.003). Percent ω‐3 fatty acid (eicosapentanoic + docosahexanoic acids) and percent arachidonic acid also were found to be inversely related to the risk of seminal vesicle involvement (OR = 0.52, 95% CI, 0.30–0.90; P = 0.02; and OR = 0.84, 95% CI,; 0.75–0.95; P = 0.005, respectively).CONCLUSIONSProstatic PUFA levels appear to influence the risk of locally advanced prostate carcinoma in men with clinically organ‐confined disease. This association may be mediated through the immune system. Cancer 2004. © 2004 American Cancer Society.
Range sustainment for the future
Authors: Haliscak Jonathan P. 
Published: October 2004

AbstractTechnological advances have resulted in weapons systems with the ability to precisely hit targets at great range. To reduce potential safety hazards of such weapons, larger and larger areas are required to test these munitions, and for personnel to train with them. This has resulted in competition for the space the military requires to test and train with these weapons, and the space needed by growing municipalities and commercial activity. Further, an increasingly restrictive environmental regulatory framework—such as the Endangered Species Act—has constrained military training realism. A solution to the challenge of sustaining bases and ranges is integrated community/military planning. © 2004 Wiley Periodicals, Inc.
Tissue plasminogen activator and glial function
Authors: Gravanis Iordanis , Tsirka Stella E. 
Published: October 2004

AbstractTissue plasminogen activator (tPA) is the only FDA‐approved treatment of thrombotic stroke and is a major parenchymal serine protease in the brain. However, it has been implicated in a plethora of brain pathologies, raising concern about its use as a safe therapeutic. tPA is thought to regulate physiological processes that entail tissue remodeling and plasticity, purportedly due to its ability to initiate the degradation of extracellular matrix proteins and possibly other substrates. Understanding the physiological role(s) of tPA promises to both elucidate important aspects of brain function and improve the available therapies for neurological disease. In this context, the effects of tPA on glial cells, mainly microglial cells, but also astrocytes and Schwann cells, appear to be of particular importance, given the increasing awareness of the significance of glia in brain physiology and pathology © 2004 Wiley‐Liss, Inc.
Caveolin and GLT‐1 gene expression is reciprocally regulated in primary astrocytes: Association of GLT‐1 with non‐caveolar lipid rafts
Authors: Zschocke Jürgen , Bayatti Nadhim , Behl Christian 
Published: October 2004

AbstractCaveolae represent membrane microdomains acting as integrators of cellular signaling and functional processes. Caveolins are involved in the biogenesis of caveolae and regulate the activity of caveolae‐associated proteins. Although caveolin proteins are found in the CNS, the regulation of caveolins in neural cells is poorly described. In the present study, we investigated different modes and mechanisms of caveolin gene regulation in primary rat astrocytes. We demonstrated that activation of cAMP‐dependent signaling pathways led to a marked reduction in protein levels of caveolin‐1/‐2 in cortical astrocytes. Application of transforming growth factor‐α (TGF‐α) also resulted in a decrease of caveolin‐1/‐2 expression. Decreased caveolin protein levels were mirrored by diminished caveolin gene transcription. The repressive effect of TGF‐α on caveolin‐1 expression was MAP kinase‐independent and partly mediated through the PI3‐kinase pathway. Further downstream, inhibition of histone deacetylases abrogated TGF‐α effects, suggesting that chromatin remodeling processes could contribute to caveolin‐1 repression. Intriguingly, alterations of caveolin gene expression in response to cAMP or TGF‐α coincided with reciprocal and brain‐region specific changes in glial glutamate transporter GLT‐1 expression. The reciprocal regulation of caveolin‐1 and GLT‐1 expression might be gated through a common PI3‐kinase dependent pathway triggered by TGF‐α. Finally, we showed that GLT‐1 is located in non‐caveolar lipid rafts of cortical astrocytes. In conclusion, this study highlights the occurrence of the reciprocal regulation of caveolin and GLT‐1 expression during processes such as astrocyte differentiation via common signaling pathways. We also provide strong evidence that GLT‐1 itself is concentrated in lipid rafts, inferring an important role for glial glutamate transporter function. © 2004 Wiley‐Liss, Inc.
Increased expression of the astrocytic glutamate transporter GLT‐1 in the prefrontal cortex of schizophrenics
Authors: Matute Carlos , Melone Marcello , Vallejo‐Illarramendi Ainara , Conti Fiorenzo 
Published: October 2004

AbstractTo verify whether altered glial glutamate uptake contributes to the reduced efficacy of glutamatergic transmission reported in the prefrontal cortex of schizophrenics, we studied the expression of GLT‐1, the transporter responsible for most glutamate transport, in autoptic samples of prefrontal cortex using real time quantitative RT‐PCR, immunocytochemistry, and functional assays. GLT‐1 mRNA levels in medication‐free patients were 2.5‐fold higher than in controls, whereas they were normal or reduced in patients treated with antipsychotics. We also observed a 4‐fold increase in L‐[3H]‐Glu uptake in Xenopus oocytes injected with mRNA from the prefrontal cortex of a medication‐free schizophrenic and a 2‐fold increase in GLT‐1 protein in the same cortical area of another medication‐free patient. Results suggest that GLT‐1 mRNA, protein and function are increased in prefrontal cortex of schizophrenics. © 2004 Wiley‐Liss, Inc.
5‐Hydroxytryptamine activates a barium‐sensitive, cAMP‐mediated potassium conductance in the leech giant glial cell
Authors: Britz Frank C. , Hirth Ingolf C. , Schneider Hans‐Peter , Deitmer Joachim W. 
Published: October 2004

Abstract5‐Hydroxytryptamine (5‐HT), a neurotransmitter and neuromodulator in the central nervous system of the leech Hirudo medicinalis hyperpolarizes the giant glial cell in the neuropil of segmental ganglia at micromolar concentrations. The 5‐HT‐evoked glial response (EC50 ≈2.5 μM) is mediated by a non–desensitizing, G‐protein‐coupled receptor and due to activation of a Ca2+‐independent K+ conductance. The adenylyl cyclase inhibitor SQ22,536 blocks the response to 5‐HT; in the presence of 1 mM db‐cAMP, but not of 1 mM db‐cGMP, the glial response is suppressed. The 5‐HT‐evoked response is reduced by Ba2+ with half‐maximal inhibition at 50 μM Ba2+. The results suggest that release of 5‐HT from serotonergic neurons, or the maintenance of micromolar levels of extracellular 5‐HT in the ganglion, may help to set the glial membrane potential close to the K+ equilibrium potential. © 2004 Wiley‐Liss, Inc.
Involvement of adenylate cyclase and tyrosine kinase signaling pathways in response of crayfish stretch receptor neuron and satellite glia cell to photodynamic treatment
Authors: Uzdensky Anatoly , Kolosov Mikhail , Bragin Denis , Dergacheva Olga , Vanzha Olga , Oparina Lidiya 
Published: October 2004

AbstractNeuroglial interactions are most profound during development or damage of nerve tissue. We studied the responses of crayfish stretch receptor neurons (SRN) and satellite glial cells to photosensitization with sulfonated aluminum phthalocyanine Photosens. Although Photosens was localized mainly in the glial envelope, neurons were very sensitive to photodynamic treatment. Photosensitization gradually inhibited and then abolished neuron activity. Neuronal and glial nuclei shrank. Some neurons and glial cells lost the integrity of the plasma membrane and died through necrosis after the treatment. The nuclei of other glial cells but not neurons become fragmented, indicating apoptosis. The number of glial nuclei around neuron soma increased, probably indicating proliferation for enhanced neuron protection. Adenylate cyclase (AC) inhibition by MDL‐12330A, or tyrosine kinase (TK) inhibition by genistein, shortened neuron lifetime, whereas AC activation by forskolin or protein tyrosine phosphatases (PTP) inhibition by sodium orthovanadate prolonged neuronal activity. Therefore, cAMP and phosphotyrosines produced by AC and TK, respectively, protected SRN against photoinactivation. AC inhibition reduced photodamage of the plasma membrane and subsequent necrosis in neuronal and glial cells. AC activation prevented apoptosis in photosensitized glial cells and stimulated glial proliferation. TK inhibition protected neurons but not glia against photoinduced membrane permeabilization and subsequent necrosis whereas PTP inhibition more strongly protected glial cells. Therefore, both signaling pathways involving cAMP and phosphotyrosines might contribute to the maintenance of neuronal activity and the integrity of the neuronal and glial plasma membranes. Adenylate cyclase but not phosphotyrosine signaling pathways modulated glial apoptosis and proliferation under photooxidative stress. © 2004 Wiley‐Liss, Inc.
Complexation of retroviruses with charged polymers enhances gene transfer by increasing the rate that viruses are delivered to cells
Authors: Landázuri Natalia , Le Doux Joseph M. 
Published: October 2004

AbstractBackgroundWe have previously found that retrovirus transduction is enhanced when an anionic polymer (chondroitin sulfate C) is added to virus stocks that contain an equal weight concentration of a cationic polymer (Polybrene). This observation was unexpected given that previous work has shown that cationic polymers enhance transduction while anionic polymers have the opposite effect.MethodsUsing model recombinant retroviruses and lentiviruses that encode for the Escherichia coli lacZ gene and quantitative assays of virus adsorption and transduction, we examined the mechanism of enhancement.ResultsWe found that addition of oppositely charged polymers (Polybrene and chondroitin sulfate C) to virus stocks enhanced gene transfer by increasing the flux of active viruses to the cells. Virus–polymer complexes formed that did not reduce the stability of the viruses, yet were large enough to sediment, delivering the viruses to the cells more rapidly than by simple diffusion. The size of the complexes, the rate of sedimentation, and the levels of gene transfer increased with increasing concentrations of polymers. The degree to which transduction was enhanced ranged from 2‐ to nearly 40‐fold, and varied depending on the type of cells and viruses used. Interestingly, we found that association of the viruses with the polymer complexes did not significantly hinder their ability to complete post‐binding steps of transduction.ConclusionsComplexation of retroviruses with charged polymers significantly improves the efficiency of ex vivo gene transfer by increasing the number of active viruses that reach the cells. Copyright © 2004 John Wiley & Sons, Ltd.
Each sensory nerve arising from the geniculate ganglion expresses a unique fingerprint of neurotrophin and neurotrophin receptor genes
Authors: Farbman Albert I. , Guagliardo Nick , Sollars Suzanne I. , Hill David L. 
Published: October 2004

AbstractNeurons in the geniculate ganglion, like those in other sensory ganglia, are dependent on neurotrophins for survival. Most geniculate ganglion neurons innervate taste buds in two regions of the tongue and two regions of the palate; the rest are cutaneous nerves to the skin of the ear. We investigated the expression of four neurotrophins, nerve growth factor (NGF), brain‐derived neurotrophic factor (BDNF), neurotrophin 3 (NT‐3), and NT‐4, and five neurotrophin receptors, trkA, trkB, trkC, p75, and truncated trkB (Trn‐B) in single sensory neurons of the adult rat geniculate ganglion associated with the five innervation fields. For fungiform papillae, a glass pipette containing biotinylated dextran was placed over the target papilla and the tracer was iontophoresed into the target papilla. For the other target fields, Fluoro‐Gold was microinjected. After 3 days, geniculate ganglia were harvested, sectioned, and treated histochemically (for biotinylated dextran) or immunohistochemically (for Fluoro‐Gold) to reveal the neurons containing the tracer. Single labeled neurons were harvested from the slides and subjected to RNA amplification and RT‐PCR to reveal the neurotrophin or neurotrophin receptor genes that were expressed. Neurons projecting from the geniculate ganglion to each of the five target fields had a unique expression profile of neurotrophin and neurotrophic receptor genes. Several individual neurons expressed more than one neurotrophin receptor or more than one neurotrophin gene. Although BDNF is significantly expressed in taste buds, its primary high affinity receptor, trkB, was not prominently expressed in the neurons. The results are consistent with the interpretation that at least some, perhaps most, of the trophic influence on the sensory neurons is derived from the neuronal somata, and the trophic effect is paracrine or autocrine, rather than target derived. The BDNF in the taste bud may also act in a paracrine or autocrine manner on the trkB expressed in taste buds, as shown by others. © 2004 Wiley‐Liss, Inc.
Noradrenaline up‐regulates the neuronal and the inducible nitric oxide synthase isoforms in magnocellular neurons of rat brain slices
Authors: Grange‐Messent Valérie , Raison Danièle , Dugas Bernard , Calas André 
Published: October 2004

AbstractNitric oxide (NO) and noradrenaline (NA) are suggested to be implicated in the regulation of neuropeptide secretion in the supraoptic nuclei (SON) and the paraventricular nuclei (PVN) of the hypothalamus. Our study demonstrates short‐term interactions between NA and the activity and expression of NO synthase (NOS) in magnocellular neurons, by using an ex vivo model of hypothalamic slices. In the SON as well as in the PVN, total NOS activity exhibited a time‐dependant increase after an incubation with NA. In the SON, this increase of total NOS activity was in part the consequence of stimulation of the iNOS activity. Coimmunodetections showed that cells expressing the inducible form of NOS were not astrocytes but magnocellular neurons. Steady‐state levels of iNOS and nNOS mRNA were dramatically enhanced by NA, particularly in the SON. Consequently, we provide new evidence that iNOS could play an important role in multiple physiological functions, including extracellular fluid balance, lactation, and parturition. © 2004 Wiley‐Liss, Inc.
The proof of a conjecture of Bouabdallah and Sotteau
Authors: Xu Min , Hou Xinmin , Xu Jun‐Ming 
Published: October 2004

AbstractLet G be a connected graph of order n. A routing in G is a set of n(n − 1) fixed paths for all ordered pairs of vertices of G. The edge‐forwarding index of G, π(G), is the minimum of the maximum number of paths specified by a routing passing through any edge of G taken over all routings in G, and πΔ,n is the minimum of π(G) taken over all graphs of order n with maximum degree at most Δ. To determine πn−2p−1,n for 4p + 2⌈p/3⌉ + 1 ≤ n ≤ 6p, A. Bouabdallah and D. Sotteau proposed the following conjecture in [On the edge forwarding index problem for small graphs, Networks 23 (1993), 249–255]. The set 3 × {1, 2, … , ⌈(4p)/3⌉} can be partitioned into 2p pairs plus singletons such that the set of differences of the pairs is the set 2 × {1, 2, … , p}. This article gives a proof of this conjecture and determines that πn−2p−1,n is equal to 5 if 4p + 2⌈p/3⌉ + 1 ≤ n ≤ 6p and to 8 if 3p + ⌈p/3⌉ + 1 ≤ n ≤ 3p + ⌈(3p)/5⌉ for any p ≥ 2. © 2004 Wiley Periodicals, Inc. NETWORKS, Vol. 44(4), 292–296 2004
Desminopathies in muscle disease
Authors: Paulin Denise , Huet Alexis , Khanamyrian Luiza , Xue Zhigang 
Published: October 2004

AbstractA recently identified class of myopathies is produced by abnormal desmin, and is characterized by a disorganization of the desmin filament network, the accumulation of insoluble desmin‐containing aggregates, and destructive changes in the sarcomeric organization of striated muscles. The desmin filaments interact with various other cytoskeletal proteins. The distinct clinical phenotypes are heterogeneous, with progressive skeletal myopathy, cardiomyopathy, and respiratory insufficiency as the most prominent features. Most of the desmin mutations are autosomal dominant. Identification of the causal genetic mutations shows that the desmin gene is not the only gene implicated in desminopathies; other genes encoding desmin‐associated proteins, such as alpha‐B‐crystallin, and synemin may also be involved. Patients with mutations in their alpha‐B‐crystallin gene, which produce similar skeletal and cardiac myopathies, also have opaque lenses. Knockout mice have helped to reveal the fundamental role of desmin filaments in cell architecture, sarcomere alignment, myofibril organization, and the distribution of mitochondria. Transgenic mice, which accumulate aggregates of desmin and associated proteins in their muscles, show that the loss of desmin intermediate function as a result of mutations in desmin itself, or in the desmin‐associated constituents, is important for disease progression. Copyright © 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
The keratin cytoskeleton in liver diseases
Authors: Zatloukal Kurt , Stumptner Conny , Fuchsbichler Andrea , Fickert Peter , Lackner Carolin , Trauner Michael , Denk Helmut 
Published: October 2004

AbstractThe keratin intermediate filament (IF) cytoskeleton of hepatocytes has continuously gained medical relevance over the last two decades. Originally it was mainly recognized as a differentiation marker for diagnostic purposes in pathology. However, keratin IFs were soon identified as major cellular structures to be affected in a variety of chronic liver diseases, such as alcoholic and non‐alcoholic steatohepatitis (ASH, NASH), copper toxicosis, and cholestasis. Based on observations in keratin gene knock‐out mice, the insight into the functional role of keratins was extended from a mere structural role providing mechanical stability to hepatocytes, to an additional role as target and modulator of toxic stress and apoptosis. The functional relevance of keratins in human diseases has recently been underlined by the identification of mutations in keratin genes in patients with liver cirrhosis. Copyright © 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
The cytoskeleton and disease
Authors: Ramaekers Frans CS , Bosman Fred T 
Published: October 2004

AbstractCytoskeletal research in recent years has revolutionized cell biology and biomedicine. The cytoskeleton spans the cytoplasm and interconnects the cell nucleus with the extracellular matrix, thereby forming a structural link between molecules involved in cell communication on the one hand, and gene expression on the other. Since the cytoskeleton is involved in virtually all cellular processes, abnormalities in this essential cellular component frequently result in disease. In this introduction, the basic structure of the cytoskeleton is briefly outlined. Furthermore, the disease processes in which the cytoskeleton plays a decisive role, and which are reviewed in detail in the papers in this issue, are briefly introduced. The advances in our understanding of the cytoskeleton and its function in disease will lead to new diagnostic and therapeutic applications in the foreseeable future. Copyright © 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.