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PubMed1986

The arachidonic acid cascade is involved in the masculinizing action of testosterone on embryonic external genitalia in mice.

We have evaluated whether the arachidonic acid cascade may be involved in the folding and fusion of the penis and scrotum in masculine differentiation, a possibility raised by recent observations of the involvement of the arachidonic acid cascade in the analogous embryonic processes of elevation and fusion of the palatal shelves and of folding and fusion of the neural tube. To test this hypothesis, during embryonic masculine differentiation in mice of the B10.A strain, we administered certain agents that produce blockade of masculinization. We report that arachidonic acid can reverse the inhibition of masculine development in male embryos produced by estradiol-17 beta or by cyproterone acetate, an androgen receptor-site blocker, and that such reversal can be prevented by an inhibitor of cyclooxygenase, such as indomethacin. We have also found that agents that block the arachidonic acid cascade at the level of phospholipase A2 (cortisone, phenytoin) or at the level of cyclooxygenase (indomethacin, aspirin) also block masculine differentiation and that such antimasculinization is reversed by arachidonic acid. The masculinization of male embryos is inhibited by indomethacin and aspirin, and the masculinization of female embryos produced by exogenous testosterone is prevented by indomethacin. These findings provide evidence that the mechanism by which testosterone organizes the genitalia involves a role of the arachidonic acid cascade leading to prostaglandins at a critical period of development and that interference with testosterone synthesis or action leads to a teratogenic deficiency of arachidonic acid during this time in the genital anlagen.

Animals↗

PubMed1988

Arachidonic acid cascade metabolites in porcine E. coli shock. Coagulation, fibrinolytic and hemodynamic response.

Cardiopulmonary hemodynamics and changes in various hemostatic factors (alpha 2M, alpha 2AP, AT III, prothrombin-proconvertin activity, fibrinogen concentration, ethanol gelation test and fibrinolytic activity on fibrin plates) were investigated in pigs during shock induced with live Escherichia coli. Anesthetized pigs were treated with indomethacin or with the combined cyclooxygenase/lipoxygenase inhibitor BW755C before the E. coli infusion or were left untreated as septic controls. Septic shock developed in all of these animals. Pretreatment attenuated the early deterioration of pulmonary circulation but did not modify the coagulation/fibrinolytic activation or the disturbed cardiopulmonary hemodynamics seen in the delayed phase of shock. The arachidonic acid cascade metabolites thus seems to mediate the early, but not the delayed cardiopulmonary reaction and to have minor importance for activation of coagulation and fibrinolysis in E. coli-shocked pigs.

Animals↗

PubMed1997

Collection of three bacterial aerosols by respirator and surgical mask filters under varying conditions of flow and relative humidity.

A variety of respirator filters and surgical masks were challenged with three aerosolized bacteria: Mycobacterium abscessus (M.a.) (a rod), Staphylococcus epidermidis (S.e.) (a sphere), and Bacillus subtilis (B.s.) (a rod). Tests were conducted at two flow rates (45 and 85 l./min) and two humidity levels (30 and 70%). Aerosols were measured with a total-particle, direct-reading, spectrometer and a viable particle cascade impactor. Measurements up- and downstream of the filter or mask were used in determining aerosol penetration; respirator or surgical mask fit was not evaluated. Bioaerosol penetration measured with two aerosol sampling instruments was found to correlate. Additionally, bioaerosol test parameters were evaluated with respect to their effect on penetration. Increasing flow resulted in increased penetration of all organisms while an increase in relative humidity did not exert a consistent effect on all organisms. Of the respirators approved by the National Institute for Occupational Safety and Health (NIOSH), filter efficiency was as expected with dust/mist respirators having the lowest and HEPA filters the highest efficiency. Surgical masks were the least efficient of all filters tested; these are not certified by NIOSH. Bioaerosol penetration was compared to that of a polystyrene latex sphere (PSL) aerosol. Penetration of the test aerosols was predicted on the basis of particle aerodynamic diameter and was expected to be in this order: PSL > M.a. > S.e. = B.s. The PSL aerosol was the most penetrating, as predicted. However, results showed that B.s. was more penetrating than S.e. The aerodynamic diameter may not be the best parameter for predicting aerosol penetration of non-spherical particles in these filters.

Aerosols↗

PubMed1994

Activation of blood clotting factors by microbial proteinases.

There are very few reports on the involvement of bacterial proteinases on the blood clotting system using both human plasma and purified clotting factors. We studied whether microbial proteinases from the opportunistic pathogens Candida albicans, Pseudomonas aeruginosa and Serratia marcescens activate the blood clotting cascade by using normal human plasma, human plasmas deficient in clotting factor XII or X, and also by using purified clotting factors XII, X and prothrombin. All proteinases tested activated either clotting factor XII or prothrombin in vitro, thus resulting in generation of thrombin. Clotting factor X was converted to the active form (Xa) by both Candida and Pseudomonas proteinases, but not by Serratia proteinase. These results suggest that peripheral and systemic blood circulation may be impaired by activation of the blood clotting cascade by microbial infections, especially in septic patients, which would enhance disseminated intravascular coagulation and multi-organ failure.

Amino Acid Sequence↗

PubMed2004

Moderate hypothermia in the management of severe traumatic brain injury: a good idea proved ineffective?

Many drugs with proven efficacy in the preclinical stage have failed to show any benefit in improving the outcome of severe traumatic brain injury (TBI) when tested in controlled clinical trials. Hypothermia is still the most powerful neuroprotective method in experimental models of TBI. Its ability to influence the multiple biochemical cascades that are set in motion after TBI is quite unique. In experimental models hypothermia protects against mechanical neuronal and axonal injury and improves behavioral outcome. Encouraging results from phase II and III clinical trials of hypothermia in TBI reported in the 1990s generated great enthusiasm. However, enthusiasm faded in 2001 after the final report of the multicenter phase III trial in which the neuroprotective effects of moderate hypothermia in TBI were formally tested. This study found no significant effect on outcome in the hypothermia group, leading many clinicians to lose interest in this therapy. The present article reviews the historical background of the use of hypothermia, presents the rationale for using both immediate and deferred hypothermia, and summarizes both experimental and clinical evidence supporting its potential benefits in the management of severe TBI. New technologies using intravascular methods to induce fast hypothermia have recently become available. Cooling either through the intravenous or intra-arterial route is an exciting alternative with great potential. We argue that moderate hypothermia is still the most powerful neuroprotective candidate for severe TBI and that it merits further research and discussion. We also defend the need for further clinical trials to prove or refute its potential for treating high intracranial pressure refractory to first level therapeutic measures. The premature abandonment of hypothermia could close new avenues for improving the devastating effects of TBI.

Animals↗

PubMed2001

Human medulloblastoma cell line DEV is a potent tool to screen for factors influencing differentiation of neural stem cells.

The aim of our study was to investigate whether a human neural cell line could be used as a reliable screening tool to examine the functional conservation, in humans, of transcription factors involved in neuronal or glial specification in other species. Gain-of-function experiments were performed on DEV cells, a cell line derived from a human medulloblastoma. Genes encoding nine different transcription factors were tested for their influence on the process of specification of human DEV cells towards a neuronal or glial fate. In a first series of experiments, DEV cells were transfected with murine genes encoding transcription factors known to be involved in the neuronal differentiation cascade. Neurogenins-1, -2, and -3; Mash-1; and NeuroD increased the differentiation of DEV cells towards a neuronal phenotype by a factor of 2-3.5. In a second series of experiments, we tested transcription factors involved in invertebrate glial specification. In the embryonic Drosophila CNS, the development of most glial cells depends on the master regulatory gene glial cell missing (gcm). Expression of gcm in DEV cells induced a twofold increase of astrocytic and a sixfold increase of oligodendroglial cell types. Interestingly, expression of tramtrack69, which is required in all Drosophila glial cells, resulted in a fourfold increase of only the oligodendrocyte phenotype. Expression of the related tramtrack88 protein, which is not expressed in the fly glia, or the C. elegans lin26 protein showed no effect. These results show that the Drosophila transcription factor genes tested can conserve their function upon transfection into the human DEV cells, qualifying this cell line as a screening tool to analyze the mechanisms of neuronal and glial specification.

Animals↗

PubMed1981

Soluble and particulate activators of complement and granulomatous pulmonary reactions.

In order to test the hypothesis that the histological changes of extrinsic allergic alveolitis result from non-specific activation of the complement cascade we studied pulmonary reactions to equivalent doses of soluble and particulate activators of complement in rats. A single intratracheal instillation of zymosan, a particulate activator of the complement system, produced a florid granulomatous pneumonitis which was maximal at 5 days. This granulomatous reaction did not appear to be associated with the development of hypersensitivity to zymosan. Complement depletion by cobra venom factor did not suppress the granulomatous reaction. Equivalent doses of soluble activators of complement failed to produce any inflammatory changes in the lung. Large doses of immune complex produced an acute, complement dependent, haemorrhagic alveolitis which was maximal at 8 hr and which resolved completely by 48 hr. We conclude that the late granulomatous pulmonary reaction to intra-tracheally administered zymosan is not due to an immune response, or a consequence of direct activation of the alternative pathway of complement, but is of 'foreign body' type. We urge caution in drawing conclusions regarding the pathogenesis of the allergic alveolitides on histological appearances alone.

Alveolitis, Extrinsic Allergic↗

PubMed2005

Is there a spatial association between senile plaques and neurofibrillary tangles in Alzheimer's disease?

OBJECTIVE: To test the hypothesis that the clusters of senile plaques (SP) and neurofibrillary tangles (NFT) in patients with Alzheimer's disease (AD) are spatially associated as predicted by the 'Amyloid Cascade Hypothesis'. METHODS: The spatial association between the SP and NFT was studied in the cerebral cortex and hippocampus in six cases of sporadic Alzheimer's disease (AD) using contingency tables. The coefficient C7 was used as an index of spatial association while chi-square with correction for continuity was used as a test of significance. RESULTS: In the brain regions analysed, values of C7 were in the range -0.31 to +0.32 but a statistically significant spatial association between SP and NFT was present in only 8/39 (21%) regions. The degree of spatial association between the SP and NFT was similar in different brain regions and did not vary with apolipoprotein e genotype of the patient. However, the magnitude of C7 in a region was positively correlated with the density of the NFT and with the total density of SP and NFT but not with the density of SP alone. CONCLUSION: There was little evidence that SP and NFT were spatially associated except in brain areas with high densities of lesions. The data support the hypothesis that SP and NFT are distributed relatively independently in the cerebral cortex and hippocampus and therefore, could be distinct phenomena in AD.

Aged↗

PubMed2004

Activation of cAMP signaling facilitates the morphological maturation of newborn neurons in adult hippocampus.

Previous studies have demonstrated that activation of the cAMP cascade, including the cAMP response element-binding protein (CREB), increases the proliferation and survival of newborn neurons in adult mouse hippocampus. In the present study, we determined whether the cAMP-CREB cascade also influences the morphological maturation of newborn neurons in the subgranular zone of the hippocampus. Rolipram, a selective inhibitor of the cAMP-specific phosphodiesterase type 4, was administered to activate the cAMP cascade, and neuronal morphology was determined by analysis of Golgi-impregnated neurons in the subgranular zone of hippocampus. Rolipram administration significantly increased the number of branch points and length of dendrites relative to vehicle treatment. Increased branch number and length were accompanied by increased levels of phosphorylated CREB, the active form of this transcription factor, in immature neurons. In contrast, the morphology of Golgi-impregnated neurons was not significantly influenced by rolipram treatment in inducible transgenic mice expressing a dominant-negative mutant of CREB in hippocampus. We also tested the influence of cAMP analogs in primary hippocampal cultures and found that activation of the cAMP pathway increased and inhibition of the cAMP cascade decreased the number of branches and length of processes as observed in vivo. These findings indicate that the cAMP-CREB cascade plays an important role in the differentiation and maturation of newborn neurons in hippocampus.

Animals↗

PubMed2004

Diagnosis of the antiphospholipid syndrome: how far to go?

The past decade has seen an evolution in the way that thrombophilic conditions are diagnosed and understood. This has largely evolved through the detection of single nucleotide polymorphisms in critical regulating proteins that are thought to confer significant structural-functional changes at key points in the coagulation cascade. The antiphospholipid syndrome (APS) is a complex hypercoagulable disorder that as yet defies the possibility of simple, predictive testing.

Antibodies, Antiphospholipid↗

PubMed2003

Effects of transient loss of shear stress on blood-brain barrier endothelium: role of nitric oxide and IL-6.

Loss of blood-brain barrier (BBB) function may contribute to post-ischemic cerebral injury by yet unknown mechanisms. Ischemia is associated with anoxia, aglycemia and loss of flow (i.e. shearing forces). We tested the hypothesis that loss of shear stress alone does not acutely affect BBB function due to a protective cascade of mechanisms involving cytokines and nitric oxide (NO). To determine the relative contribution of shear stress on BBB integrity we used a dynamic in vitro BBB model based on co-culture of rat brain microvascular endothelial cells (RBMEC) and astrocytes. Trans-endothelial electrical resistance (TEER), IL-6 release and NO levels were measured from the lumenal and ablumenal compartments throughout the experiment. Flow-exposed RBMEC were challenged with 1 h of normoxic-normoglycemic flow cessation (NNFC) followed by reperfusion for 2 to 24 h. NNFC caused a progressive drop in nitric oxide production during flow cessation followed by a time-dependent increase in ablumenal IL-6 associated with a prolonged NO increase during reperfusion. The nitric oxide synthetase (NOS) inhibitor L-NAME (10 microM) abrogated all effects of NNFC, including changes in NO and cytokine production. BBB permeability did not increase during or after NNFC/reperfusion, but was increased by treatment with L-NAME or when the effects of IL-6 were blocked. Flow adapted RBMEC and astrocytes respond to NNFC/reperfusion by overproduction of IL-6, possibly secondary to increased production of NO during the reperfusion. Maintenance of BBB function during and following NNFC appears to depend on intact NO signaling and IL-6 release.

Animals↗

PubMed1991

Technetium 99m radiolabeling of aerosolized drug particles from metered dose inhalers.

To assess mechanisms of bronchodilation and effectiveness of metered dose inhalers, it may be useful to determine sites of drug deposition in the lung. To establish suitable test aerosols, two brands of metered dose inhalers containing bronchodilator (Brethaire, Proventil) were radiolabeled with technetium ( 99mTc) and tested to determine if the distribution of radioisotope in the aerosol was representative of the distribution of agonist activity. Cascade impaction was used to determine the particle size distribution of the radioisotope and drug aerosols by assaying each state of the cascade using scintillation and HPLC techniques. Possible influences of the radiolabeling method and delivery techniques on the particle distribution were assessed by analyzing distributions from nonradiolabeled inhalers using HPLC. For these drugs, there was an excellent correlation between the distribution of radioactivity and the drug within the captured aerosol (Brethaire r = 0.994, Proventil r = 0.998, 20 - 200 consecutive puffs). Distributions were close to log-normal and differences in mass median aerodynamic diameter (MMAD) between the radioisotope and agonist activities were not significant (Brethaire, MMAD +/- sigma g, radiolabel vs drug = 4.7 +/- 2.1 mum, vs 4.4 +/- 1.7 mum, and Proventil, 2.5 +/- 2.1 mum, vs 2.4 +/- 2.0 mum. Non-labeled inhalers produced similar drug distributions (Brethaire, 4.2 +/- 1.8 mum, and Proventil 2.0 +/- 1.9 mum). Pausing between actuations resulted in slightly smaller distributions (Brethaire, 3.6 +/- 1.8 mum, Proventil 1.8 +/- 1.8 mum, 20 puffs-60 sec pauses) but the differences were not significant. In addition, to search for multimodal distributions and assess the accuracy of the MMAD measurement via our cascade impactor (Delron), we also measured the distribution of the mass of material within the aerosols using a weight-sensitive cascade (California Measurements). Using the latter device (1 puff), the mass distributions of both aerosols were similar to the values obtained from the puffs with pauses (Brethaire 3.8 +/- 2.3 mum, Proventil 1.4 +/- 2.2 mum). Multi-modal distributions were not found. By all assessments, the distributions were nearly log-normal with drug activity well described by the radiolabel.

Bronchodilator Agents↗

PubMed1987

Comparative effects of quinolones on human mononuclear leucocyte functions.

The effects of three quinoline derivatives--pefloxacin, ciprofloxacin and ofloxacin--were investigated in mitogen-stimulated human peripheral blood mononuclear leucocytes (MNL). At concentrations of 50 mg/l or more, pefloxacin, ciprofloxacin or ofloxacin significantly inhibited MNL proliferation in response to phytohaemagglutinin. This inhibition was more marked with ciprofloxacin than pefloxacin or ofloxacin. To determine the possible mechanism(s) involved in the inhibition of MNL proliferation following exposure to pefloxacin, ciprofloxacin or ofloxacin, we assessed (1) interleukin-1 (IL-1) activity in supernatants from monocytes treated with the quinolones and (2) the effects of 2-mercaptoethanol (2-ME) a thiol compound which acts as an antioxidant agent and the effect of indomethacin (INDO) an inhibitor of prostaglandin E2 synthesis. 2-ME and INDO did not prevent the decrease in the proliferation. IL-1 activity was shown to be decreased for the same range of antibiotic concentrations as observed for the inhibition of MNL proliferation. Cellular viability of the MNL or monocytes was not modified by any of the quinolones at the concentrations tested. Taken together, these results suggest that pefloxacin, ciprofloxacin and ofloxacin act as immunomodulators. The mechanism involved with the cascade of events that leads to the lymphocyte proliferation and the clinical relevance need further investigation.

Cell Survival↗

PubMed2003

Enhancement of fibrinolytic potential in vitro by anticoagulant drugs targeting activated factor X, but not by those inhibiting thrombin or tissue factor.

Tissue factor-induced coagulation leads to the generation of a small amount of thrombin, resulting in the formation of a fibrin clot. After clot formation, thrombin generation continues resulting in the activation of thrombin activatable fibrinolysis inhibitor, leading to downregulation of fibrinolysis. In this study, the effect of anticoagulant drugs targeting different steps in the coagulation cascade on clot formation and subsequent breakdown was investigated using a plasma-based clot lysis assay. All drugs tested significantly delayed clot formation; only those drugs targeting activated factor X (FXa) (tissue factor pathway inhibitor, fondaparinux, and low molecular weight heparin) accelerated fibrinolysis. Anticoagulant drugs targeting tissue factor (active site-inactivated recombinant activated factor VII) or thrombin (hirudin and d-phenylalanyl-l-prolyl-l-arginyl chloromethyl ketone) did not affect clot lysis time. In accordance with these findings, it was shown that total thrombin generation, as quantified by the endogenous thrombin potential, was only affected by anticoagulant drugs targeting FXa when all drugs were used in a concentration resulting in doubling of clotting time. Induction of hyperfibrinolysis by anticoagulant drugs directed against FXa might be beneficial as increased clot breakdown might facilitate thrombolysis or prevent re-occlusion. On the other hand, the induction of hyperfibrinolysis by these compounds might increase the risk of bleeding complications.

Amino Acid Chloromethyl Ketones↗

PubMed1992

Effect of hypothermia on the coagulation cascade.

BACKGROUND AND METHODS: The development of a multifactorial coagulopathy after massive transfusion is a well-recognized clinical problem that is almost always accompanied by hypothermia. The purpose of this study was to investigate the isolated effect of alterations of temperature on the integrity of the coagulation cascade. Prothrombin times and partial thromboplastin times were each performed 15 times on samples of pooled normal plasma at the temperatures of 37 degrees C, 34 degrees C, 31 degrees C, and 28 degrees C, as well as 39 degrees C and 41 degrees C. RESULTS: Mean prothrombin time results increased from 11.8 +/- 0.3 (SD) secs at 37 degrees C to 12.9 +/- 0.5, 14.2 +/- 0.5, and 16.6 +/- 0.2 secs at 34 degrees C, 31 degrees C, and 28 degrees C, respectively (p < or = .001 for each). Partial thromboplastin time determinations increased from 36.0 +/- 0.7 (SD) secs at 37 degrees C to 39.4 +/- 1.0, 46.1 +/- 1.1, and 57.2 +/- 0.6 secs at 34 degrees C, 31 degrees C, and 28 degrees C, respectively (p < or = .001 for each). Both prothrombin time and partial thromboplastin time determinations were only minimally shortened at hyperthermic temperatures. CONCLUSIONS: The series of enzymatic reactions of the coagulation cascade are strongly inhibited by hypothermia, as demonstrated by the dramatic prolongation of prothrombin time and partial thromboplastin time tests at hypothermic deviations from normal temperature in a situation where factor levels were all known to be normal. Clinicians who deal with critically ill massively transfused hypothermic patients all recognize the inevitable appearance of a coagulopathy that has a multifactorial origin. Unless specifically considered, the contribution of hypothermia to the hemorrhagic diathesis may be overlooked since coagulation testing is performed at 37 degrees C, rather than at the patient's actual in vivo temperature.

Blood Coagulation Disorders↗

PubMed1990

Ground-based air-sampling measurements near the Nevada Test Site after atmospheric nuclear tests.

Historical air-sampling data measured within 320 km (200 mi) of the Nevada Test Site (NTS) have been reviewed for periods following atmospheric nuclear tests, primarily in the 1950s. These data come mostly from high-volume air samplers, with some from cascade-impactor samplers. Measurements considered here are for beta radiation from gross fission products. The resulting air-quality data base is comprised of almost 13,000 samples from 42 sampling locations downwind of the NTS. In order to compile an accurate air-quality data base for use in estimating exposure via inhalation, raw data values were sought where possible, and the required calculations were performed on a computer with state-of-the-art algorithms. The data-processing procedures consisted of (1) entry and error checking of historical data; (2) determination of appropriate background values, air-sampling volumes, and net air concentrations; and (3) calculation of integrated air concentration (C) for each sample (considering fallout arrival times). Comparing C values for collocated high-volume and cascade-impactor samplers during the Upshot-Knothole series showed similar lognormal distributions, but with a geometric mean C for cascade impactors about half that for the high-volume air samplers. Overall, the uncertainty in C values is about a factor of three. In the past, it has been assumed that C could be related to ground deposition by a constant having units of velocity. In our data bases, simultaneous measurements of air concentration and ground deposition at the same locations were not related by a constant; indeed, there was a great amount of scatter. This suggests that the relationship between C and ground deposition in this situation is too complex to be treated adequately by simple approaches.

Air Pollutants, Radioactive↗

PubMedDate not supplied

Effects of nonionic contrast media (CM) on the components of coagulation and complement systems.

Several nonionic experimental contrast media (CM) were evaluated for their effects on coagulation cascade, platelet aggregation, and the activation of complement pathways. In an in vitro system, most of the contrast media tested showed a mild anticoagulant property by prolonging the clotting times, such as partial thromboplastin time and the thrombin time of pooled normal human plasma. However, aggregation of normal human platelets by adenosine-diphosphate (ADP), collagen, epinephrine, ristocetin, and thrombin was not blocked when the platelet-rich plasma was incubated with these agents. No quantitative or qualitative changes in the complement components C3 or C4 were detected when a mixture of CM and pooled normal human serum was analyzed by radial immunodiffusion, immuno- or crossed-immunoelectrophoresis techniques. These results indicate that nonionic contrast media produce certain transient hematologic changes and should be further tested for their immunologic properties in order to establish their absolute safety in diagnostic procedures.

Blood Coagulation↗

PubMed2003

Family history of gastric cancer: should we test and treat for Helicobacter pylori?

A close link has been established between infection and gastric cancer. In this article, we suggest that using a risk stratification technique (like that for colorectal cancer), the high-risk group of first-degree relatives of patients with gastric cancer can be separated out for testing and treatment. This would be more manageable and more cost-effective than screening the whole population, in which the mortality from distal gastric cancer has declined concomitant with the eradication of infection. Support for the feasibility of this approach is derived from studies showing that the family is the core unit of transmission and that childhood colonization, especially with a virulent strain, is apparently a major risk factor for disease progression to the neoplastic stage. When there is a case of gastric cancer in the family, first-degree relatives, who might be infected by a bacterium with an identical genetic fingerprint, are at higher risk than normal for developing gastric cancer. Furthermore, genetic and epidemiologic studies based on the Correa model have shown that both primary and secondary prevention of gastric cancer is possible. Calculations done in high-risk populations, such as Japanese-Americans, confirm the savings in cost and the safety of the test-and-treat strategy. Considering that eradication should be done as early as possible, at a point in the cascade when the changes are still reversible, and that gastric cancer is associated with a high mortality rate, we suggest that this strategy be applied to this high-risk population.

Helicobacter Infections↗