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En la ya no tan reciente historia argentina de la última dictadura aparecen dos textos–Prensa clandestinade Rodolfo Walsh, según recopilación de Horacio Verbitsky (1976–1978) y Cuerpo a cuerpode David Viñas (1979)–documental uno, ficcional el otro, que ponen en escena la dialéctica benjaminiana de que “Jamás se da un documento cultural sin que lo sea al mismo tiempo de la barbarie”.

Human immunodeficiency virus (HIV)-infection is characterized by loss of CD4+ T cells associated with high levels of immune activation, T-cell proliferation, and lymphocyte apoptosis. To investigate the role of intrinsic perturbations of cell-cycle control in the immunopathogenesis of acquired immunodeficiency syndrome (AIDS), we studied the expression of cell-cycle–dependent proteins in lymphocytes from HIV-infected patients. Cyclin B1 expression, Nucleolar Organizer Regions (NORs) number, and NORs area of distribution were all consistently increased in HIV-infected patients, but returned to normal after effective antiretroviral therapy, suggesting that viral replication is directly implicated in the genesis of the observed changes. Analysis of cyclin B1 intracellular turnover showed that the increased cyclin B1 expression is (1) caused by defective degradation in the presence of normal rates of synthesis, and (2) is temporally associated with decreased levels of ubiquitination. After in vitro activation of lymphocytes from healthy individuals, cyclin B1 and cdc25 expression and ubiquitination, p34 cdc2 activity, NORs morphology, and C23/nucleolin localization showed a 72- to 96-hour cyclic pattern that led to a biologic state similar to baseline. On the contrary, complex but consistent changes of the same indices followed activation of T lymphocytes from HIV-infected patients, resulting in a 5-fold increase in apoptosis. Overall, our data indicate that a profound dysregulation of cell-cycle control is present in lymphocytes from HIV-infected patients. This finding may provide a novel biologic link between immune activation, accelerated lymphocyte turnover, and increased apoptosis during HIV infection.

Human immunodeficiency virus (HIV)-infection is characterized by loss of CD4+T cells associated with high levels of immune activation, T-cell proliferation, and lymphocyte apoptosis. To investigate the role of intrinsic perturbations of cell-cycle control in the immunopathogenesis of acquired immunodeficiency syndrome (AIDS), we studied the expression of cell-cycle–dependent proteins in lymphocytes from HIV-infected patients. Cyclin B1 expression, Nucleolar Organizer Regions (NORs) number, and NORs area of distribution were all consistently increased in HIV-infected patients, but returned to normal after effective antiretroviral therapy, suggesting that viral replication is directly implicated in the genesis of the observed changes. Analysis of cyclin B1 intracellular turnover showed that the increased cyclin B1 expression is (1) caused by defective degradation in the presence of normal rates of synthesis, and (2) is temporally associated with decreased levels of ubiquitination. After in vitro activation of lymphocytes from healthy individuals, cyclin B1 and cdc25 expression and ubiquitination, p34 cdc2 activity, NORs morphology, and C23/nucleolin localization showed a 72- to 96-hour cyclic pattern that led to a biologic state similar to baseline. On the contrary, complex but consistent changes of the same indices followed activation of T lymphocytes from HIV-infected patients, resulting in a 5-fold increase in apoptosis. Overall, our data indicate that a profound dysregulation of cell-cycle control is present in lymphocytes from HIV-infected patients. This finding may provide a novel biologic link between immune activation, accelerated lymphocyte turnover, and increased apoptosis during HIV infection.

HIV infection is marked by the progressive destruction of the CD4 T lymphocyte subset, an essential component of the immune system and a vital source of cytokines required for differentiation of natural killer (NK) and ?? T cells, for maturation of B lymphocytes into plasmocytes, and for differentiation of CD8T cells into virus-specific cytotoxic T lymphocytes. CD4 T lymphocytes are also a source of chemokines which control migration of lymphocytes to the site of infection and which also inhibit HIV entry into CD4-expressing targets. Continuous production of viral proteins leads to an unbalanced immune activation and to the triggering of apoptotic programs, turning mononuclear cells, including CD4 T cells, CD8 T cells and APC, into effectors of apoptosis, leading to fratricidal destruction of healthy uninfected cells expressing the death receptors. Inappropriate PCD is also responsible for the disappearance of T helper cells primed for type-1 cytokine synthesis, thus contributing to the lack of survival factors which could prevent spontaneous lymphocyte apoptosis. Under potent anti-retroviral therapies, a significant decrease in spontaneous, TCR- and CD95-induced lymphocyte apoptosis is observed, concomitant with a partial quantitative and qualitative restoration of the immune system in treated patients. However, owing to the suppressive effect of anti-retroviral drugs on physiological apoptosis, these therapies are associated with alteration of TNF-?-regulated T cell homeostasis, leading to an accumulation in the blood of T cells primed for TNF-? synthesis, and contributing to the development of a new syndrome associated with these treatments, the lipodystrophy syndrome.

Background:Lymphocyte function associate-1 (LFA-1), macrophage antigen-1 (Mac-1), and very late activation antigen-4 (VLA-4) are involved in the infiltration of leukocytes into the tissues. Experimental models of allergic inflammation suggest that VLA-4 could determine the selective recruitment of eosinophils into the inflamed airways. Objective:Our purpose was to evaluate the involvement of integrins in eosinophil recruitment in asthma. Methods:We evaluated by immunocytochemistry the expression of VLA-4, LFA-1, and Mac-1 and their relationship with inflammatory cells and severity of disease in the induced sputum of 20 mild to moderate atopic asthmatic subjects and in 8 healthy subjects. Results:The number of VLA-4+ cells is increased in asthmatic patients and VLA-4 is mainly localized on eosinophils. Furthermore, VLA-4+ cells are significantly related to eosinophils. In contrast, LFA-1 and Mac-1 cellular expressions do not differ between asthmatic and control subjects and are not related to any specific cell type. Eosinophils and VLA-4+ cells are significantly higher in moderately compared with mildly asthmatic patients (P< .01, P< .05) and with healthy control subjects (P< .0005, P< .001). Eosinophils and VLA-4+ cells are also higher in mildly asthmatic patients compared with control subjects (P< .001, P< .005). Conclusion:This is the first report demonstrating, by a noninvasive method in humans, that VLA-4+ cells are increased and correlate with the eosinophils in the induced sputum of atopic patients with mild to moderate asthma and that VLA-4 expression is related to the severity of disease. (J Allergy Clin Immunol 2000;105:65-70.)

Tuberculosis (TB) is still a major health problem, both as a single disease entity and as a cofactor in AIDS. The interaction between macrophage and Mycobacterium tuberculosis(MTB) is a critical step in the establishment of an early chronic infection. This study analyses the capacity of MTB to induce apoptosis in cells obtained by broncho‐alveolar lavage (BAL) from patients with reactive pulmonary tuberculosis and from AIDS patients with disseminated pulmonary tuberculosis. Apoptosis was increased three‐fold in BAL cells obtained from patients with pulmonary tuberculosis and even more markedly in alveolar macrophages of MTB‐infected AIDS patients, compared with controls. Apoptosis was analysed and characterized by propidium iodide (PI) incorporation, terminal deoxy transferase (TDT)‐mediated dUTP‐biotin nick end labelling (TUNEL), and tissue transglutaminase (tTG) expression. The MTB–macrophage interaction was also investigated in vitroby infecting monocyte‐derived macrophages (MDM) with MTB (virulent strain H37Rv). The induction of apoptosis by MTB required viable bacteria, was dose‐dependent, and was restricted to H37Rv. Infection with either Mycobacterium aviumcomplex (MAC) or HIV‐1 and treatment with heat‐killed MTB failed to induce apoptosis. © 1997 by John Wiley & Sons, Ltd.

Tuberculosis (TB) is still a major health problem, both as a single disease entity and as a cofactor in AIDS. The interaction between macrophage and Mycobacterium tuberculosis (MTB) is a critical step in the establishment of an early chronic infection. This study analyses the capacity of MTB to induce apoptosis in cells obtained by broncho-alveolar lavage (BAL) from patients with reactive pulmonary tuberculosis and from AIDS patients with disseminated pulmonary tuberculosis. Apoptosis was increased three-fold in BAL cells obtained from patients with pulmonary tuberculosis and even more markedly in alveolar macrophages of MTB-infected AIDS patients, compared with controls. Apoptosis was analysed and characterized by propidium iodide (PI) incorporation, terminal deoxy transferase (TDT)-mediated dUTP-biotin nick end labelling (TUNEL), and tissue transglutaminase (tTG) expression. The MTB–macrophage interaction was also investigated in vitro by infecting monocyte-derived macrophages (MDM) with MTB (virulent strain H37Rv). The induction of apoptosis by MTB required viable bacteria, was dose-dependent, and was restricted to H37Rv. Infection with either Mycobacterium avium complex (MAC) or HIV-1 and treatment with heat-killed MTB failed to induce apoptosis. © 1997 by John Wiley & Sons, Ltd.

The activation of T-lymphocytes through the recognition of specific allergens is a crucial event in the development of allergic inflammation. Dendritic cells (DC) are potent accessory cells that play an important role in initiating bronchial immune responses by activation of T-lymphocytes. We investigated the distribution of CD1a+ DC in the bronchial biopsies from asthmatic patients, and evaluated the effects of a short course of low dose inhaled fluticasone propionate treatment. Twenty-three mild to moderate stable asthmatic patients and eight normal subjects were included in the study. Bronchoscopy with bronchial biopsies were performed in each subject. Eighteen of the 23 asthmatics underwent a second bronchoscopy after 6 weeks of low dose inhaled fluticasone propionate treatment (250 mcg bd) in a placebo-controlled double-blind study. Biopsies were embedded into glycolmethacrylate resin and analysed by immunohistochemistry methods using specific monoclonal antibodies against CD1a, which is a widely recognized marker for DC. In asthmatics, CD1a+ DC number was significantly higher in bronchial epithelium (P<0.001) and in lamina propria (P<0.001) when compared with normal controls. In addition, we observed that a short course of low dose inhaled fluticasone propionate treatment decreased the number of CD1a+ DC in both the bronchial epithelium (P<0.05) and lamina propria (P<0.01). The increased number of CD1a+ DC support the hypothesis that DC play an important role in the modulation of the immune response in chronic asthma. Short-term low dose fluticasone propionate treatment induces down-regulation of the CD1a+ DC number.

Data regarding the best treatment for spontaneous coronary artery dissection (SCAD) are limited. Theaim of the present study was to compare the clinical outcomesof conservative versusinvasive treatment in SCAD patients.

La puntuación de calcio arterial coronario (CAC) mejora la precisión de la estratificación del riesgo de enfermedad cardiovascular ateroesclerótica (ECVA) en comparación con los factores de riesgo cardiovascular tradicionales. Se evaluó la interacción de la carga ateroesclerótica coronaria determinada por la puntuación de CAC con el beneficio pronóstico de los tratamientos hipolipemiantes en el contexto de la prevención primaria.

Prognosis in pulmonary hypertension is strictly linked to right ventricle failure, which results from uncoupling between right ventricle function and its afterload. This study sought to describe how to estimate with echocardiography right ventricular wall tension, its correlation with right ventricle haemodynamics and its prognostic role. A total of 190 patients without overt right ventricle failure but with suspected pulmonary hypertension on a previous echocardiogram underwent right heart catheterization and nearly-simultaneous echocardiography. Right ventricular wall tension was estimated according to Laplace’s law as right ventricle length × tricuspid regurgitation peak gradient and it was correlated with right ventricle haemodynamic profile; its potential prognostic impact was tested along with canonical right ventricle function parameters. Right ventricular wall tension correlated significantly with invasive estimation of right ventricle end-diastolic pressure (R: 0.343, p< 0.001) and with several other haemodynamic variables, such as mean pulmonary artery pressure, pulmonary artery compliance, transpulmonary gradient, pulmonary vascular resistance, right atrial pressure and right ventricle stroke work index (all p< 0.001). At a mean follow-up of five years and three months, only right ventricular wall tension was associated to all-cause mortality (p= 0.036), while tricuspid annular plane systolic excursion (p= 0.536), right ventricle fractional area change (p= 0.383), right ventricle fractional area change (p= 0.076), tricuspid regurgitation peak gradient (p= 0.107) and tricuspid annular plane systolic excursion/tricuspid regurgitation peak gradient (p= 0.181) could not. We identified a novel bedside echocardiographic predictor of altered right ventricle haemodynamics, which is precociously altered in patients without overt right ventricle failure and is associated to all-cause mortality at a long-term follow-up. Further studies are needed to confirm its role in pulmonary hypertension patients.

AbstractVenom of the hyperparasitoid Asaphes lucens(Provancher) immediately paralyzed and stopped development of the larva of the aphid parasitoid Aphidius smithiSharma and Subba Rao, which did not void a meconium and deteriorated into a soft, blackened mass. On the other hand, venom of a second hyperparasitoid, Dendrocerus carpenteri(Curtis), did not immediately paralyze the larva of A. smithi, which developed up to the prepupal stage, voided a meconium, and remained bright yellow for up to 4–6 weeks before decaying.

Several letters to the editor are presented in response to the articles published in the previous issues of the journal including "Passenger Capacity Question" by David Feinberg of Seattle, Washington.

Treatment with tumor necrosis factor-alpha (TNF-alpha) inhibitors increases the risk of tuberculosis (TB) due to reactivation of latent Mycobacterium tuberculosis infection (LTBI). Screening for LTBI is based mainly on the tuberculin skin test (TST), which has several limitations in any patient who is immunosuppressed due to drugs or autoimmune disease. T cell interferon-gamma release assays (IGRA) have been shown to be more specific than TST in immunocompetent patients and potentially represent a new approach for the management of patients taking TNF-alpha blockers. Even if there is no evidence-based literature of IGRA superiority versus TST in this specific clinical setting, some studies suggest blood assays may be helpful in clinical management of these patients, in addition to currently recommended clinical screening for risk factors for LTBI.

Purpose: Accurate prognostication is essential to guide clinical management in patients with pulmonary arterial hypertension (PAH). The goal of this study is to provide a comprehensive overview of the most thoroughly evaluated echocardiographic findings aiming to predict adverse outcome in PAH. Methods: MEDLINE and EMBASE electronic databases were systematically searched for longitudinal studies published by April 2015 that reported associations between echocardiographic findings and adverse clinical outcome in PAH. Studies were appraised using previously developed criteria for prognostic studies. Meta-analysis of echocardiographic findings investigated by ≥4 studies was performed using random effect models. In case of significant heterogeneity (I²>50% or Cochran’s Q p-value <0.10) additional sensitivity analyses were performed by excluding specific patient subgroups. Results: Thirty-seven papers investigating 6669 patients were included. Pooled hazard ratios and heterogeneity statistics are shown in the table. For TR severity and RV free wall LPSS no statistical heterogeneity was found, however the reported standard errors were generally larger. Sensitivity analyses did not change the overall results and conclusions for pericardial effusion, right atrial area and TAPSE. These results can be therefore regarded with a higher degree of certainty. Conclusions: This meta-analysis substantiates the clinical yield of specific echocardiographic findings in the prognostication of PAH patients in day-to-day practice. Especially, pericardial effusion, right atrial area and TAPSE are of prognostic value. Systematic review registration number: CRD42014009231. Prognostic value of echo findings in PAH No. of studiesHazard ratio95% CIp-valueI², %Cochran's Q (p-value)Presence of pericardial effusion161.701.44-1.99<0.0014225.7 (0.041)Right atrial area, per 5 cm² increase51.711.38-2.13<0.001558.9 (0.063)RV systolic pressure, per 10 mmHg increase71.181.01-1.380.0437625.1 (<0.001)Tricuspid regurgitation severity72.201.64-2.95<0.001399.8 (0.133)Right atrial pressure, >15 mmHg62.451.56-3.85<0.0017620.7 (<0.001)TAPSE, per 5 mm increase70.580.46-0.75<0.0017726.1 (<0.001)RV fractional area change, per 5% increase50.810.69-0.960.0396010.1 (0.039)Tei index, per 0.1 unit increase71.231.09-1.400.0017322.3 (0.001)RV free wall longitudinal peak systolic strain, per 5% increase41.721.53-1.93<0.00103.0 (0.392)

Context.The synchrotron radio morphology of bilateral supernova remnants depends on the mechanisms of particle acceleration and on the viewing geometry. However, unlike X-ray and γ-ray morphologies, the radio emission does not depend on the cut-off region of the parent electron population, making it a simpler and more straightforward tool to investigate the physics of cosmic ray production in supernova remnants (SNRs).

Context.Observations of SuperNova Remnants (SNRs) in X-ray and γ-ray bands promise to contribute important information to our understanding of the kinematics of charged particles and magnetic fields in the vicinity of strong non-relativistic shocks and, therefore, the nature of Galactic cosmic rays. The accurate analysis of SNR images collected in different energy bands requires theoretical modeling of synchrotron and inverse Compton emission from SNRs.

Context. X-ray observations have proven to be very effective in detecting previously unknown supernova remnant shells around pulsar wind nebulae (PWNe), and in these cases the characteristics of the shell provide information about the evolutionary stage of the embedded PWN. However, it is not clear why some PWNe are “naked”.Aims. We perform an X-ray observational campaign targeting the PWN G54.1+0.3, the “close cousin” of the Crab Nebula, to try to detect the associated SNR shell.Methods. We analyze XMM-Newton and Suzaku observations of G54.1+0.3 to model the contribution of a dust scattering halo.Results. We detecte an intrinsic faint diffuse X-ray emission surrounding the PWN out to ~ 6' (~10 pc) from the pulsar, characterized by a hard spectrum, which can be modeled with either a power law (γ= 2.9) or a thermal plasma model (kT= 2.0 keV.)Conclusions. Assuming the shell to be thermal, we derive an explosion energy E= 0.5–1.6×1051erg, a pre-shock ISM density of 0.2 cm-3, and an age of ~2000 yr. Using these results in the MHD model of PWN-SNR evolution, we obtain excellent agreement between the predicted and observed location of the shell and PWN shock.

Context. X-ray observations have proven to be very effective in detecting previously unknown supernova remnant shells around pulsar wind nebulae (PWNe), and in these cases the characteristics of the shell provide information about the evolutionary stage of the embedded PWN. However, it is not clear why some PWNe are “naked”.

Context. X-ray emitting features originating from the interaction of supernova shock waves with small interstellar gas clouds are revealed in many X-ray observations of evolved supernova remnants (e.g., Cygnus Loop and Vela), but their interpretation is not straightforward.Aims. We develop a self-consistent method for the analysis and interpretation of shock-cloud interactions in middle-aged supernova remnants, which can provide the key parameters of the system and the role of relevant physical effects such as thermal conduction, without the need to perform ad-hoc numerical simulations and bother about morphology details.Methods. We explore all the possible values of the shock speed and cloud density contrast relevant to middle-aged SNRs with a set of hydrodynamic simulations of shock-cloud interaction including the effects of thermal conduction and radiative cooling. From the simulations, we synthesize spatially and spectrally resolved focal-plane data as they would be collected with XMM-Newton/EPIC, an X-ray instrument commonly used in these studies.Results. We develop and calibrate two diagnostic tools, the first based on the mean photon energy versus count-rate scatter plot and the second on the spectral analysis of the interaction region, that can be used to highlight the effects of thermal conduction and to derive the shock speed in case of efficient conduction at work. These tools can be used to ascertain information from X-ray observations, without the need to develop detailed and ad-hoc numerical models for the interpretation of the data.

Context. X-ray emitting features originating from the interaction of supernova shock waves with small interstellar gas clouds are revealed in many X-ray observations of evolved supernova remnants (e.g., Cygnus Loop and Vela), but their interpretation is not straightforward.

Context. Recent SuzakuX-ray observations of the ejecta-dominated supernova remnant W49B have shown that there is a clear indication in the global spectrum for overionized plasma, whose physical origin is still under debate.

Context. Recent SuzakuX-ray observations of the ejecta-dominated supernova remnant W49B have shown that there is a clear indication in the global spectrum for overionized plasma, whose physical origin is still under debate.Aims. In order to ascertain the physical origin of this rapidly cooling plasma, we focus on its spatial localization within the X-ray emitting ejecta.Methods. We confirm a saw-edged excess (interpreted as a strong radiative recombination continuum) in the global spectrum above 8 keV, which emerges above the ionization-equilibrium model. We produce a hardness-ratio map to determine where the plasma is overionized and perform a spectral analysis of the regions with and without strong overionization.Results. We find that the overionized plasma is localized in the center of the remnant and in its western jet, while it is not detected in the bright eastern jet, where the expansion of the ejecta is hampered by their interaction with a dense interstellar cloud.Conclusions. The location of overionized plasma suggests that the inner ejecta are rapidly cooling by expansion, unlike the outer ejecta, for which expansion is hampered by interstellar clouds seen in H2.

Several letters to the editor are presented in response to articles in previous issues including "Making the Climb," in the June 2009 issue, "Intrusion Detection and Prevention on IBM i" in the March 2009 issue, and "Open Up the Possibilities" in the February 2009 issue.

ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 200 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.

Several letters to the editor are presented in response to articles in previous issues including "Mastering Table Topics," by Bob Leo in the April 2008 issue, "Speaking to an All-Women Audience...When You're a Man," by Neil Chethik in the April 2008 issue and "Remedy for a Lifeless Speech" in the March 2008 issue.

Presents an interview of Robert Bocchino, president of DeVry College of Technology in North Brunswick, New Jersey. Effort toward partnership with employers to provide high technology job training; Necessity of public funds for the improvement of technology education; Connections of Bocchino on public policy.

Discusses the need for high-tech graduates in New Jersey. Challenge for New Jersey employers and the higher-education community; Search for graduates with solid technical foundation combined with strong interpersonal and communication skills; Need for colleges and universities to provide a relevant education in high-demand industries.