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At least 1,189 records · Page 66Linked to original sources
PubMed2002

Benzodiazepine-induced superoxide signals B cell apoptosis: mechanistic insight and potential therapeutic utility.

The properties of a proapoptotic 1,4-benzodiazepine, Bz-423, identified through combinatorial chemistry and phenotype screening are described. Bz-423 rapidly generated superoxide (O(2)(-)) in transformed Ramos B cells. This O(2)(-) response originated from mitochondria prior to mitochondrial transmembrane gradient collapse and opening of the permeability transition pore. Bz-423-induced O(2)(-) functioned as an upstream signal that initiated an apoptotic program characterized by cytochrome c release, mitochondrial depolarization, and caspase activation. Pretreatment of cells with agents that either block the formation of Bz-423-induced O(2)(-) or scavenge free radicals attenuated the death cascade, which demonstrated that cell killing by Bz-423 depends on O(2)(-). Parallels between Ramos cells and germinal center B cells prompted experiments to determine whether Bz-423 had therapeutic activity in vivo. This possibility was tested using the (NZB x NZW)F(1) murine model of lupus, in which the pathologically enhanced survival and expansion of germinal center B cells mediate disease. Administration of Bz-423 for 12 weeks specifically controlled germinal center hyperplasia and reduced the histological evidence of glomerulonephritis. Collectively, these studies define a new structure-function relationship for benzodiazepines and point to a new target and mechanism that could be of value for developing improved drugs to manage systemic lupus erythematosus and related disorders.

Animals↗
PubMed2002

Assessment, diagnosis and management of lower urinary tract symptoms in men.

Lower urinary tract symptoms are very common and the approach to assessment and management has changed dramatically over the past few years. Previously referred to as prostatism, benign prostatic hyperplasia and bladder outflow obstruction, it is now recognised that in most men symptoms are due to a combination of benign prostatic enlargement and age-related bladder dysfunction. Most men require only simple tests for a diagnosis, with the more complex investigations reserved for when the diagnosis is not clear. Symptom bothersomeness and effect on quality of life are the critical factors when deciding how to treat a man. A cascade of treatments exists, including conservative management, medical therapy and surgery. A man moves up the cascade when the present management strategy fails to control symptoms. Traditional surgical techniques such as transurethral resection of the prostate are still appropriate for some men, although with improved medical treatments available the number of men undergoing surgery is declining.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1991

The effect of flow on hemostasis and thrombosis.

While dilution of procoagulants has generally been proposed as the mechanism by which flow reduces coagulation at surfaces, such a mechanism has never been verified experimentally and, in fact, there are theoretical grounds for suspecting the validity of such a hypothesis (29). It is quite plausible that flow may have direct effects on certain enzyme or polymerization kinetics involved in thrombosis, in addition to the well-defined effect that flow has an enhancing transport of reactants and products to and from the vessel wall. Such effects of flow on immobilized enzymes have occasionally been observed, but never studied with respect to coagulative processes (30). The study of the effects of flow on hemostasis and thrombosis, while numerous, are still in their infancy. As noted above, increasing shear increases the rate of formation of factor Xa in a tubular reactor. In the presence of factors VIII and IX, there is also a shear-induced enhancement of Xa production (31). These studies indicate that at least some coagulation reactions are accelerated in the presence of high shear. However, it has been observed that fibrin formation is diminished at increasing shear rates (20). This implies that at least one step of the coagulation cascade is being inhibited by high shear. One possibility is that fibrin monomer is being removed by the high local flow conditions, although the concomitant reduction in fibrinopeptide A argues against this interpretation. Another possibility, not yet tested, is that thrombin itself is removed by flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Coagulation↗
PubMed1991

L-alpha-phosphatidylcholine-induced stimulation of PGI2 production in canine gallbladders following hypovolemic shock and Escherichia coli sepsis.

In vitro production of PGI2 in canine gallbladders subjected to hypovolemic shock and Escherichia coli sepsis was studied to determine whether a precursor above arachidonic acid in the cyclooxyenase cascade might be operative in the production of prostacyclin, which, in turn, may play a role in the pathogenesis of acute acalculous cholecystitis (AC). L-alpha-phosphatidylcholine (LaP), an arachidonic acid precursor, was used as the test agent. LaP did not stimulate PGI2 production from either gallbladder surface in the hypovelimic animals or the mucosa of the septic shock group. However, it did stimulate PGI2 production from the SS serosa compared with controls, 1375 +/- 432 versus 633 +/- 198 pg/cm2/min (P less than .05). In conclusion, lack of stimulation of PGI2 in the hypovolemic model suggests that PGI2 does not play a role in AC. Alternatively, it may play a role in preventing this disease process in septic shock. This study demonstrates the use of precursors of arachidonic acid and the cyclooxygenase pathway as active participants in the production of PGI2, although it is unclear whether the prostacyclin produced helps prevent AC in septic shock.

Acute Disease↗
PubMed1995

Thrombin generation in plasma: its assessment via the endogenous thrombin potential.

Thrombin generation is a pivotal function of plasma in haemostasis and thrombosis. Its mechanism is essentially the classical cascade, the velocity of which is governed by the availability of factors Va and VIIIa and that is confined to the surface of the procoagulant membranes which appear at the site of injury. There is no routine test that quantitatively renders the thrombin forming capacity of a plasma sample. Clotting times (PT-prothrombin time, APTT-activated partial tromboplastin time) do not reflect the over all thrombin generation and are insensitive to hypercoagulative states. The endogenous thrombin potential (ETP), i.e. the area under the thrombin generation curve, better represents this function. We developed a method to assess the ETP in the routine laboratory. The first results suggest that it is a sensitive indicator for every form of anticoagulation. It is increased in hypercoagulable states thus far studied, both congenital and acquired and can be designed to indicate deficiencies in protein C and S and APC (activated protein C) resistance.

Animals↗
PubMed2002

Distinct sensitizing effects of the cAMP-PKA second messenger cascade on rat dural mechanonociceptors.

Activation of the cAMP/protein kinase A (PKA) second messenger cascade has been implicated in the induction of mechanical hyperalgesia by inflammatory mediators. We examined the role of this cascade in mechanical sensitization of nociceptive neurons that innervate the meninges, a process thought to be involved in the pathophysiology of headache syndromes such as migraine. Single unit activity was recorded in the trigeminal ganglion from 40 mechanosensitive dural afferents (conduction velocitity: 0.3-6.6 m s(-1)) and nine mechanically insensitive dural afferents (MIAs) (conduction velocitity: 0.3-2.8 m s(-1)) while stimulating the dura with a servo force-controlled stimulator or von Frey monofilaments, respectively. Local application to the dura of dibutyryl adenosine 3',5'-cyclic monophosphate (dbcAMP, 100 microM), a stable membrane-permeant cAMP analogue, produced mechanical sensitization in the majority of mechanosensitive units (19/29, 66 %). Two distinct patterns of mechanical sensitization were observed. Thirty-eight per cent of the units exhibited only a decrease in threshold (TH group), while 28 % showed only an increase in suprathreshold responses (STH group). dbcAMP also induced mechanosensitivity in the majority of MIA units (6/9, 67 %). dbcAMP-induced sensitization was blocked by the PKA inhibitors, Rp-cAMP (1 mM) and H-89 (100 microM). A mixture of inflammatory mediators induced both components of sensitization in the majority of mechanosensitive units tested. However, in each unit, PKA inhibitors blocked only one of the two effects (either TH or STH). Units that were classified as TH or STH also differed in their baseline stimulus-response slopes, thresholds and conduction velocities. These findings implicate the cAMP-PKA cascade in sensitization of dural mechanonociceptors and suggest that this cascade may produce sensitization through at least two different mechanisms operating in separate neuronal populations.

Animals↗
PubMed2005

Assessment of snapper (Pagrus auratus) natural IgM binding to bromelain treated sheep erythrocytes.

Normal snapper (Pagrus auratus Bloch and Schneider) serum was examined for natural IgM that binds to protease (bromelain) treated sheep erythrocytes (BrSRBC) in a model assay system that has been used to appraise natural IgM of various mammals. Normal snapper serum lysed BrSRBC while haemolysis was abrogated by heat inactivation of serum and in divalent cation-deficient conditions, indicative of classical complement mediated lysis. In addition, heat inactivated normal snapper serum agglutinated BrSRBC while phosphatidylcholine (PtC) liposomes partially inhibited both haemolysis and agglutination. Inhibition of haemolysis and agglutination may have been mediated by an interaction between immunoglobulin (Ig) and PtC as protein A purified snapper Ig bound to PtC liposomes. However it is not known if this binding was PtC specific nor if the binding was initiated by either the Fab and/or Fc domains of snapper Ig. BrSRBC plaque forming cells (PFC) were detected in the peritoneal cavity, spleen, head kidney and peripheral blood of normal snapper. The greatest proportion of BrSRBC PFC per B cell was within the peritoneal cavity followed by the spleen, peripheral blood and head kidney. Together, these data suggest that normal snapper serum may contain natural Ig that binds BrSRBC, activating the classical complement cascade.

Analysis of Variance↗
PubMed1998

Is Fanconi anemia caused by a defect in the processing of DNA damage?

Fanconi anemia (FA) is an autosomal genetic disease characterized by a complex array of developmental disorders, a high predisposition to bone marrow failure and to acute myelogenous leukemia. The chromosomal instability and the hypersensitivity to DNA cross-linking agents led to its classification with the DNA repair disorders. This review aimed at establishing whether it is still appropriate to consider 1/approximately FA within a DNA repair framework taking into account the recently discovered genetic heterogeneity characteristics of the defect (eight complementation groups). We discuss the possibility that the FA proteins interact to form a complex which may control different functions, including the processing of specific DNA lesions. Such a complex may act as a sensor to initiate protective systems as well as transcription of specific genes specifying, among others proteins, growth factors. Such steps may be organized as a linear cascade or more likely under the form of a web network.

Apoptosis↗
PubMed2000

Surface modification of the polymers present in a polysulfone hollow fiber hemodialyser by covalent binding of heparin or endothelial cell surface heparan sulfate: flow characteristics and platelet adhesion.

The present study addresses the problem of simultaneous surface modification of various polymers, i.e. polysulfone (PSU), polycarbonate (PC), and polyurethane (PU), which constitute the Ultraflux AV 600 S hollow fibre hemodialyser. An investigation was first made into six different chemical routes aimed at introducing carboxyl groups onto the surface of PSU, PC, and PU model polymers to which heparin (HE) or endothelial cell surface heparan sulfate (ESHS) was covalently bound via the reaction of residual amino groups and a coupling reagent. Carboxyl groups were introduced using three specific reactions based on their nucleophilic or electrophilic introduction into aromatic repeating units of the polymers and three non-specific carboxylation reactions, i.e. UV, heat or redoxactivation via nitrene or radical species. Concentrations of 1-20 nmol COOH groups per cm(-2) led to HE or ESHS surface concentrations corresponding to one or several layers. Two nonspecific carboxylation reactions followed by HE- or ESHS-coupling provided the lowest change in membrane pore structure according to cut off, clearance (urea, phosphate, maltose), ultrafiltration, and diafiltration assessments. In some cases the introduction of excess negatively-charged carboxyl groups and HE improved the flux properties of the modified membranes. The various methods were applied to the dialysis module. Platelet adhesion was not observed in the case of the ESHS-coating of PSU membrane at shear rates of 1050 s(-1), whereas HE and subendothelial matrix showed 56 and 100% coverage, respectively, under similar conditions. The coating of PSU or of other high-flux membranes by ESHS appears a promising method for improving membrane properties and to generate biocompatibility characteristics similar to those of natural blood vessels, i.e. inertness to platelet adhesion and no level effects for complement and intrinsic coagulation cascade activation. The ESHS coating may be used without anticoagulants.

Biocompatible Materials↗
PubMed1998

The new antidiabetic drug MCC-555 acutely sensitizes insulin signaling in isolated cardiomyocytes.

Freshly isolated adult rat ventricular cardiomyocytes have been used to characterize the action profile of the new thiazolidinedione antidiabetic drug MCC-555. Preincubation of cells with the compound (100 microM for 30 min or 10 microM for 2 h) did not modify basal 3-O-methylglucose transport, but produced a marked sensitizing effect (2- to 3-fold increase in insulin action at 3 x 10(-11) M insulin) and a further enhancement of maximum insulin action (1.8-fold). MCC-555 did not modulate autophosphorylation of the insulin receptor and tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1). However, insulin action (10(-10) and 10(-7) M) on IRS-1-associated phosphatidylinositol (PI) 3-kinase activity was enhanced 2-fold in the presence of MCC-555. Association of the p85 adapter subunit of PI 3-kinase to IRS-1 was not modified by the drug. Immunoblotting experiments demonstrated expression of the peroxisomal proliferator-activated receptor-gamma in cardiomyocytes reaching about 30% of the abundance observed in adipocytes. The insulin-sensitizing effect of MCC-555 was lost after inhibition of protein synthesis by preincubation of the cells with cycloheximide (1 mM; 30 min). Cardiomyocytes from obese Zucker rats exhibited a completely blunted response of glucose transport at 3 x 10(-11) M insulin. MCC-555 ameliorates this insulin resistance, producing a 2-fold stimulation of glucose transport, with maximum insulin action being 1.6-fold higher than that in control cells. This drug effect was paralleled by a significant dephosphorylation of IRS-1 on Ser/Thr. In conclusion, MCC-555 rapidly sensitizes insulin-stimulated cardiac glucose uptake by enhancing insulin signaling resulting from increased intrinsic activity of PI 3-kinase. Acute activation of protein expression leading to a modulation of the Ser/Thr phosphorylation state of signaling proteins such as IRS-1 may be underlying this process. It is suggested that MCC-555 may provide a causal therapy of insulin resistance by targeted action on the defective site in the insulin signaling cascade.

Animals↗
PubMed1997

Cyclooxygenase-dependent thyroid cell proliferation induced by immunoglobulins from patients with Graves' disease.

IgG associated with Graves' disease bind to the TSH receptor and alter thyroid growth and function, mainly through the stimulation of adenylyl cyclase. In addition, Graves' IgG are able to interact with the phospholipase C (PLC)/Ca2+ and phospholipase A2 (PLA2)/arachidonic acid (AA) cascades. The activation of this latter pathway leads to thyroid cell growth in vitro. The elucidation of additional mechanisms of action of Graves' IgG has made possible the identification of four subgroups of patients, characterized by IgG with different biochemical activities (extent of cAMP and AA release stimulation in in vitro assays). On the basis of these results, a novel therapeutic approach could be proposed based on the inhibition of PLA2 and AA metabolism. To test this hypothesis, the ability of IgG from 56 Graves' patients to stimulate [3H]thymidine incorporation in FRTL5 thyroid cells in the presence and absence of the cyclooxygenase inhibitor indomethacin (2.5 x 10(-6) mol/L) was measured. A significant reduction in [3H]thymidine incorporation was found (33% inhibition; P < 0.0001) upon pretreatment with indomethacin, suggesting that in vitro thyroid cell growth is regulated by cyclooxygenase metabolites. This strengthens the argument for involvement of the PLA2/AA cascade in the pathophysiology of Graves' disease and the proposal for novel selective pharmacological treatments of these patients.

Animals↗
PubMed1999

The use of the lectin Helix pomatia agglutinin (HPA) as a prognostic indicator and as a tool in cancer research.

Progress in treatment for cancer has enabled extension of the disease-free interval, and of the quality of life for patients, but there has been very little improvement in overall survival rates. The main reason for this has been the ineffectiveness of current therapies to kill all the cancer cells once they have spread to distant sites to form metastatic deposits. One marker which has proved to be useful in identifying those cancers which have the potential to spread is the lectin Helix pomatia agglutinin (HPA). In clinical studies, HPA binding to primary tumours in tissue sections has been of prognostic value in breast, colon and gastric cancer, while no prognostic significance for HPA could be detected in tumours of the head and neck. These studies hence indicate that HPA is best suited to recognise a glycotope on adenocarcinomas. In several studies, HPA reactivity is equal or superior to other classical markers of metastatic potential. Since HPA is a marker of prognosis at the level of individual tumour cells, human tumour cell lines were screened for their HPA positivity. When transplanted into severe combined immunodeficient (scid) mice, HPA positive human breast and colon cancer cells metastasised while HPA negative cancer cell lines in general did not. In order to define HPA binding glycotopes at the molecular level, isolated cell membrane glycoproteins were exposed to labelled HPA on nitrocellulose membranes after Western blotting procedure. The majority of the isolated cell membrane glycoproteins bound HPA indicating that not a single HPA binding glycoprotein exists, which is associated with the metastatic phenotype. Functional investigations using the human/scid mouse chimeras will aid in the identification of those HPA positive glycoproteins which are functionally involved in the metastatic cascade.

Animals↗
PubMedDate not supplied

[Structural and functional disorders of erythrocyte membranes in simulated extravehicle space work].

The experimental data on a structural-and-functional status of erythrocyte membranes in ground-based simulation of human extravehicular activity (EVA) are discussed. The changes in the structure and function of erythrocyte membrane were determined from the fixation of lipophilic ions, specific activity of ion-transporting adenosine triphosphatases and content of the products of peroxide oxidation of lipids (POL) in plasma. On exposure to hypobaric hyperoxia during real EVA the membrane status changes are associated with the activation of a cascade of POL processes.

Adenosine Triphosphatases↗
PubMed1998

Signal, noise power spectrum, and detective quantum efficiency of indirect-detection flat-panel imagers for diagnostic radiology.

The performance of an indirect-detection, active matrix flat-panel imager (FPI) at diagnostic energies is reported in terms of measured and theoretical signal size, noise power spectrum (NPS), and detective quantum efficiency (DQE). Based upon a 1536 x 1920 pixel, 127 microns pitch array of a-Si:H thin-film transistors and photodiodes, the FPI was developed as a prototype for examination of the potential of flat-panel technology in diagnostic x-ray imaging. The signal size per unit exposure (x-ray sensitivity) was measured for the FPI incorporating five commercially available Gd2O2S:Tb converting screens at energies 70-120 kVp. One-dimensional and two-dimensional NPS and DQE were measured for the FPI incorporating three such converters and as a function of the incident exposure. The measurements support the hypothesis that FPIs have significant potential for application in diagnostic radiology. A cascaded systems model that has shown good agreement with measured individual pixel signal and noise properties is employed to describe the performance of various FPI designs and configurations under a variety of diagnostic imaging conditions. Theoretical x-ray sensitivity, NPS, and DQE are compared to empirical results, and good agreement is observed in each case. The model is used to describe the potential performance of FPIs incorporating a recently developed, enhanced array that is commercially available and has been proposed for testing and application in diagnostic radiography and fluoroscopy. Under conditions corresponding to chest radiography, the analysis suggests that such systems can potentially meet or even exceed the DQE performance of existing technology, such as screen-film and storage phosphor systems; however, under conditions corresponding to general fluoroscopy, the typical exposure per frame is such that the DQE is limited by the total system gain and additive electronic noise. The cascaded systems analysis provides a valuable means of identifying the limiting stages of the imaging system, a tool for system optimization, and a guide for developing strategies of FPI design for various imaging applications.

Equipment Design↗
PubMed1997

Activation of the cAMP transduction cascade contributes to the mechanical hyperalgesia and allodynia induced by intradermal injection of capsaicin.

1. The spinal role of the cAMP transduction cascade in nociceptive processing was investigated in awake behaving rats (male, Sprague-Dawley) by activating or inhibiting this pathway spinally. Microdialysis fibres were implanted into the dorsal horn to infuse drugs directly to the spinal cord. 2. Animals, without peripheral tissue injury, were tested for responses to repeated applications (10 trials) of von Frey filaments and threshold to mechanical stimulation before and after infusion of 8-bromo-cAMP. In this group of animals treated spinally with 8-br-cAMP (1-10 mM) a dose-dependent hyperalgesia and allodynia were produced. This was manifested as an increased number of responses to 10 trials of von Frey filaments (10, 50, 150, 250 mN) and a decrease in mechanical threshold. 3. A second series of experiments studied the manipulation of the cAMP pathway spinally in a model of tissue injury induced by intradermal injection of capsaicin. Animals were either pre- or post-treated spinally with the adenylate cyclase inhibitor, tetrahydrofuryl adenine (THFA) or the protein kinase A inhibitor, myrosilated protein kinase (14-22) amide (PKI). Injection of capsaicin resulted in an increased number of responses to repeated applications of von Frey filaments and a decrease in threshold to mechanical stimuli outside the site of injection, secondary mechanical hyperalgesia and allodynia. 4. Pre-treatment with either THFA (1 mM) or PKI (5 mM) had no effect on the capsaicin-evoked secondary hyperalgesia and allodynia. 5. In contrast, post-treatment spinally with THFA (0.01-1 mM) or PKI (0.05-50 mM) dose-dependently reduced the mechanical hyperalgesia and allodynia produced by capsaicin injection. Furthermore, the mechanical hyperalgesia and allodynia blocked by the adenylate cyclase inhibitor, THFA (1 mM), was reversed by infusion of 8-bromo-cAMP (0.01-10 mM) in a dose-dependent manner. 6. Thus, this study demonstrates that activation of the cAMP transduction cascade at the spinal cord level results in mechanical hyperalgesia and allodynia and that the secondary mechanical hyperalgesia and allodynia following intradermal injection of capsaicin is mediated by this same transduction cascade.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1991

Differential involvement of the arachidonic acid cascade on the alpha 1-adrenergic potentiation of vasoactive intestinal peptide- versus beta-adrenergic-stimulated cyclic AMP and cyclic GMP accumulation in rat pinealocytes.

In the rat pineal gland, alpha 1-adrenergic agonists, which stimulate arachidonic acid release, also potentiate vasoactive intestinal peptide (VIP)- or beta-adrenergic-stimulated cyclic AMP (cAMP) and cyclic GMP (cGMP) accumulation. In this study, the possible involvement of the arachidonic acid pathway in the potentiation mechanism was examined in dispersed rat pinealocytes using two inhibitors of the arachidonic acid cascade, indomethacin and nordihydroguaiaretic acid. These two inhibitors appeared to have differential effects on the alpha 1-adrenergic potentiation of VIP- or beta-adrenergic-stimulated cAMP and cGMP responses. Whereas nordihydroguaiaretic acid was effective in suppressing both the alpha 1-adrenergic potentiation of VIP- or beta-adrenergic-stimulated cAMP and cGMP responses, indomethacin inhibited selectively the VIP-mediated cAMP and cGMP responses. The role of arachidonic acid metabolites was further determined using several prostaglandins--A2, I2, E2, and F2 alpha--and leukotrienes--B4, C4, and D4. Of the seven compounds tested, prostaglandins E2 and F2 alpha stimulated basal cAMP but not cGMP accumulation. The prostaglandin E2- and F2 alpha-stimulated cAMP responses were additive to those stimulated by VIP or beta-adrenergic receptors. The other five compounds had no effects on basal or VIP- or beta-adrenergic-stimulated cAMP or cGMP accumulation. Taken together, these findings indicate that the arachidonic acid cascade is likely involved in the alpha 1-adrenergic potentiation of VIP- or beta-adrenergic-stimulated cAMP and cGMP accumulation. However, the specific arachidonic acid metabolite involved in the potentiation mechanisms of VIP- versus beta-adrenergic-stimulated cyclic nucleotide responses may be different.

Animals↗
PubMed2005

Solitary chemoreceptor cell proliferation in adult nasal epithelium.

Nasal trigeminal chemosensitivity in mice and rats is mediated in part by solitary chemoreceptor cells (SCCs) in the nasal epithelium (Finger et al., 2003). Many nasal SCCs express the G-protein alpha-gustducin as well as other elements of the bitter-taste signaling cascade including phospholipase Cbeta2, TRPM5 and T2R bitter-taste receptors. While some populations of sensory cells are replaced throughout life (taste and olfaction), others are not (hair cells and carotid body chemoreceptors). These experiments were designed to test whether new SCCs are generated within the epithelium of adult mice. Wild type C57/B6 mice were injected with the thymidine analog 5-bromo-2'-deoxyuridine (BrdU) to label dividing cells. At various times after injection (1-40 days), the mice were perfused with 4% paraformaldehyde and prepared for dual-label immunocytochemistry. Double labeled cells were detected as early as 3 days post BrdU injection and remained for as long as 12 days post-injection suggesting that SCCs do undergo turnover like the surrounding nasal epithelium. No BrdU labeled cells were detected after 24 days suggesting relatively rapid replacement of the SCCs.

Animals↗