Massive Star Formation

This chapter reviews progress in the field of massive star formation. It focuses on evidence for accretion and current models that invoke high accretion rates. In particular it is noted that high accretion rates will cause the massive young stellar object to have a radius much larger than its eventual main sequence radius throughout much of the accretion phase. This results in low effective temperatures which may provide the explanation as to why luminous young stellar objects do not ionized their surroundings to form ultra-compact H II regions. The transition to the ultra-compact H II region phase would then be associated with the termination of the high accretion rate phase. Objects thought to be in a transition phase are discussed and diagnostic diagrams to distinguish between massive young stellar objects and ultra-compact H II regions in terms of line widths and radio luminosity are presented.Comment: 21 pages, 6 figures, chapter in Diffuse Matter from Star Forming Regions to Active Galaxies - A Volume Honouring John Dyson, Edited by T.W. Hartquist, J. M. Pittard, and S. A. E. G. Falle. Series: Astrophysics and Space Science Proceedings. Springer Dordrecht, 2007, p.6

Star clusters near and far; tracing star formation across cosmic time

© 2020 Springer-Verlag. The final publication is available at Springer via https://doi.org/10.1007/s11214-020-00690-x.Star clusters are fundamental units of stellar feedback and unique tracers of their host galactic properties. In this review, we will first focus on their constituents, i.e.\ detailed insight into their stellar populations and their surrounding ionised, warm, neutral, and molecular gas. We, then, move beyond the Local Group to review star cluster populations at various evolutionary stages, and in diverse galactic environmental conditions accessible in the local Universe. At high redshift, where conditions for cluster formation and evolution are more extreme, we are only able to observe the integrated light of a handful of objects that we believe will become globular clusters. We therefore discuss how numerical and analytical methods, informed by the observed properties of cluster populations in the local Universe, are used to develop sophisticated simulations potentially capable of disentangling the genetic map of galaxy formation and assembly that is carried by globular cluster populations.Peer reviewedFinal Accepted Versio

The separation of the stars in the binary nucleus of the planetary nebula Abell 35

The definitive version is available at www.blackwell-synergy.com. Copyright Blackwell Publishing DOI : 10.1046/j.1365-8711.1998.02166.xUsing the Planetary Camera on board the Hubble Space Telescope we have measured the projected separation of the binary components in the nucleus of the planetary nebula Abell 35 to be larger than 0.08′′ but less than 0.14′′. The system was imaged in three filters centered at 2950°A, 3350°A and 5785°A. The white dwarf primary star responsible for ionizing the nebula is half as bright as its companion in the 2950°A filter causing the source to be visibly elongated. The 3350°A setting, on the other hand, shows no elongation as a result of the more extreme flux ratio. The F300W data allows the determinination of the binary’s projected separation. At the minimum distance of 160 parsec to the system, our result corresponds to 18±5 AU. This outcome is consistent with the wind accretion induced rapid rotation hypothesis, but cannot be reconciled with the binary having emerged from a common-envelope phase.Peer reviewe

Nicotinic receptor-mediated regulation of dopamine transporter activity in rat prefrontal cortex.

The objective of this study was to determine whether nicotine could selectively influence dopamine levels in the prefrontal cortex as compared with other dopaminergic areas of brain. Using a superfusion system, we found that nicotine and other agonists at nicotinic acetylcholine receptors enhanced the release of radiolabeled dopamine that was stimulated by 10 μM amphetamine from slices prepared from rat prefrontal cortex. In contrast, nicotine had no effect on amphetamine-stimulated [3H]dopamine release from slices of nucleus accumbens nor striatum. Under the conditions used, which included no added calcium to exclude contribution by exocytotic release, nicotine had no effect on basal release of [3H]dopamine. The enhancement by nicotine was concentration-dependent, reaching a maximum at 5 μM, and producing less release at higher concentrations. Enhancement by nicotine was fully reversed by 30 μM dihydro-β-erythroidine, and by 10 μM mecamylamine, but was not affected by α-bungarotoxin. The potencies of nicotine, epibatidine, cytisine, and A85380 to enhance amphetamine-stimulated dopamine release, as well as the sensitivity of nicotine enhanced release to antagonists, are consistent with mediation via a high-affinity nicotinic acetylcholine receptor containing α4 and β2 subunits, the major species of nicotinic receptor in forebrain. Since low dopaminergic activity in prefrontal cortex is correlated with cognitive deficits in schizophrenia, our findings may help explain why these deficits are improved in schizophrenics by smoking or nicotine administration. (C) 2000 Wiley-Liss, Inc

Protein kinase C regulation of dopamine transporter initiated by nicotinic receptor activation in slices of rat prefrontal cortex

We previously reported that activation of nicotinic receptors causes an enhancement in amphetamine-stimulated release of dopamine via its transporter from slices of prefrontal cortex, but no such enhancement of release from slices of nucleus accumbens or striatum. The nicotinic receptors mediating the enhancement most likely contain α4 and β2 subunits based upon pharmacological characterization. In this study, we sought to characterize the second messenger systems associated with the nicotine-mediated response. Sodium channel involvement was confirmed by the observation that tetrodotoxin blocked nicotine-mediated enhancement, whereas veratridine or elevated K+ mimicked the enhancement seen with nicotine. Inclusion of EGTA blocked nicotine-mediated enhancement, suggesting that, even though no exogenous Ca2+ was added, endogenous stores were required for the enhancement. The enhancement by nicotine was also abolished by the L-type voltage-dependent calcium channel (VDCC) antagonist nitrendipine, but not by the N-type VDCC antagonist ω-conotoxin GVIA, Finally, inhibition of protein kinase C also abolished the nicotine-mediated enhancement of amphetamine-stimulated dopamine release, whereas inhibitors of Ca2+/calmodulin kinase II did not. These findings establish that nicotine can exert selective effects on dopamine transporter activity in prefrontal cortex, an area involved in cognition and learning

Nicotinic receptor-mediated regulation of the dopamine transporter in rat prefrontocortical slices following chronic in vivo administration of nicotine

Low levels of dopaminergic activity in prefrontal cortex are thought to contribute to negative symptoms of schizophrenia. Negative symptoms are associated with the prefrontocortical area of the brain. Schizophrenic patients have a high rate of smoking, which by subjective as well as objective measures produces a cognitive benefit. We have previously shown that agonists at nicotinic receptors containing α4 and β2 subunits can enhance amphetamine-stimulated [3H]dopamine ([3H]DA) release via the dopamine transporter (DAT) from slices of rat prefrontal cortex. This effect is selective for prefrontal cortex; the enhancement does not occur in striatum or nucleus accumbens. The enhancement is dependent upon activation of protein kinase C (PKC). In the current study, we show that the enhancement of amphetamine-stimulated [3H]DA release is maintained after 10 days of chronic nicotine treatment, delivered subcutaneously twice daily. There are no significant changes in the ability of prefrontocortical brain slices to take up [3H]DA in tissue prepared from nicotine-treated vs. saline-treated rats. Nicotinic receptors mediating enhancement of amphetamine-stimulated [ 3H]DA release are at least partially localized to nerve terminals, as an enhancement in release is also observed in synaptosomal preparations. Finally, the sensitivity of the nicotine enhancement in release to the PKC inhibitor chelerythrine is also seen in synaptosomal preparations, suggesting that the signaling mechanism activated through α4β2 receptors is intact. © 2003 Elsevier Science B.V. All rights reserved

Respiratory complications in Brazilian patients infected with human immunodeficiency virus Complicações respiratórias em pacientes brasileiros infectados pelo vírus da imunodeficiência humana

PURPOSE: To determine how often and by what means an indentifiable pulmonary pathogen can be recognized in human immunodeficiency virus (HIV) infected patients with respiratory disorders in Brazil, which are the most frequently observed microorganisms and what impact specific therapy has on these agents. PATIENTS AND METHODS: Thirty-five HIV seroposiüve subjects with respiratory complaints were studied. All patients had a complete history, physical examination and blood counts. The pulmonary assessment included chest radiograms; sputum examination for bacterial and fungal pathogens; bronchoscopy with bronchoalveolar lavage and transbronchial biopsy. Patients with treatable complications received standard antimicrobial therapy. RESULTS: One or more microorganisms were found in 24 subjects and another 3 individuals showed nonspecific interstitial pneumonitis. The sputum examination identified the pulmonary pathogens in 7 cases. The bronchoalveolar lavage and the histopathologic examination were diagnostic in 14% and 83%, respectively, of the 28 individuals that were submitted to bronchoscopy. The most frequently identified microorganism was P. carinii (55%), followed by M. tuberculosis (41%) and cytomegalovirus (8%). The clinical, laboratory and radiographic findings failed to distinguish the specific pulmonary pathogens. Twenty-three individuals with P. carinii pneumonitis and/or tuberculosis received specific therapy; among the evaluable patients the therapeutic response rates were 79% for PCP and 100% for TB. CONCLUSIONS: We have determined that tuberculosis, P. carinii and cytomegalovirus pneumonitis are the most common respiratory opportunistic diseases in Brazilian patients infected with HIV. The histologic evaluation was crucial in order to identify the pulmonary pathogens. Tuberculosis in AIDS individuals displayed clinical and radiographic findings atypical for reactivation disease. However, most of the features observed in HIV infected patients had been previously described in infection of the normal host. Furthermore, the AIDS subjects showed a good therapeutic response to anti-tuberculous drugs.<br>OBJETIVO: Determinar a frequência e os meios pelos quais é possível identificar um agente patogênico respiratório em pacientes brasileiros infectados pelo vírus da imunodeficiência humana (HIV); quais são os microorganismos mais comuns; e qual é o impacto da terapêutica específica. PACIENTES E MÉTODOS: Trinta e cinco pacientes HIV positivos, com queixas respiratórias foram estudados. Todos os pacientes tiveram história, exame físico e testes hematólogicos. A avaliação da patologia respiratória incluiu radiografia pulmonar, exame do escarro para bactérias e fungos, broncoscopia com lavagem bronquiolo-alveolar e biopsia transbronquica. Pacientes com patologias tratáveis receberam a terapêutica indicada. RESULTADOS: Um ou mais organismos foram encontrados em 24 pacientes, e outros 3 pacientes mostraram pneumonite intersticial inespecífica. O exame de escarro identificou o agente patogênico pulmonar em 7 casos. O lavado bronquiolo-alveo-lar e o exame histopatológico definiram o diagnóstico em 14% e 83%, respectivamente, entre os 28 pacientes que foram submetidos à broncoscopia. O organismo mais comun foi P.carinii (55%), seguido por M.tuberculosis (41%), e citomegalovírus (8%). Os achados clínicos, laboratoriais e radioló-gicos não discriminaram os agentes patogênicos. Vinte e três pacientes com PCP ou tuberculose receberam terapêutica específica; entre os pacientes que puderam ser avaliados o tratamento foi bem sucedido em 79% dos episódios de PCP e 100% em TB. CONCLUSÕES: Determinamos que TB, PCP e CMV são as causas mais frequentes de infecções respiratórias em pacientes brasileiros infectados pelo HIV. O exame histológico foi essencial para firmar o diagnóstico etiológico. A TB em pacientes aidéticos assumiu formas semelhantes à TB primária em pacientes imunocompetentes e apresentou boa resposta terapêutica