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5. Influence of vancomycin minimum inhibitory concentration on the outcome of methicillin-susceptible Staphylococcus aureus left-sided infective endocarditis treated with antistaphylococcal β-lactam antibiotics: a prospective cohort study by the International Collaboration on Endocarditis

Author

Athan, E., Harris, O., Korman, T.M., Kotsanas, D., Jones, P., Reinbott, P., Ryan, S., Fortes, C.Q., Garcia, P., Jones, S.B., Barsic, B., Bukovski, S., Selton-Suty, C., Aissa, N., Doco-Lecompte, T., Delahaye, F., Vandenesch, F., Tattevin, P., Hoen, B., Plesiat, P., Giamarellou, H., Giannitsioti, E., Tarpatzi, E., Durante-Mangoni, E., Iossa, D., Orlando, S., Ursi, M.P., Pafundi, P.C., D' Amico, F., Bernardo, M., Cuccurullo, S., Dialetto, G., Covino, F.E., Manduca, S., Della Corte, A., De Feo, M., Tripodi, M.F., Baban, T., Kanafani, Z.A., Kanj, S.S., Sfeir, J., Yasmine, M., Morris, A., Murdoch, D.R., Premru, M.M., Lejko-Zupanc, T., Almela, M., Ambrosioni, J., Azqueta, M., Brunet, M., Cervera, C., De Lazzari, E., Falces, C., Fuster, D., Garcia-de-la-Mària, C., Garcia-Gonzalez, J., Gatell, J.M., Marco, F., Miró, J.M., Moreno, A., Ortiz, J., Ninot, S., Paré, J.C., Pericas, J.M., Quintana, E., Ramirez, J., Sandoval, E., Sitges, M., Tolosana, J.M., Vidal, B., Vila, J., Bouza, E., Muñoz, P., Rodríguez-Créixems, M., Ramallo, V., Bradley, S., Wray, D., Steed, L., Cantey, R., Peterson, G., Stancoven, A., Woods, C., Corey, G.R., Reller, L.B., Fowler, V.G., Jr., Chu, V.H., Baloch, K., Dixon, C.C., Harding, T., Jones-Richmond, M., Pappas, P., Park, L.P., Redick, T., Stafford, J., Anstrom, K., Bayer, A.S., Cabell, C.H., Karchmer, A.W., Sexton, D.J., Wang, A., Chu, V., Durack, D.T., Eykyn, S., Moreillon, P., Olaison, L., Raoult, D., Rubinstein, E., Pericàs, J.M., Messina, J.A., Park, L., Sharma-Kuinkel, B.K., and Carugati, M.

Published
2017
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7. Clinical utility of telavancin for treatment of hospital-acquired pneumonia: focus on non-ventilator-associated pneumonia

Author

Rubinstein E, Stryjewski ME, and Barriere SL

Subjects
Infectious and parasitic diseases, RC109-216
Abstract

Ethan Rubinstein,1 Martin E Stryjewski,2 Steven L Barriere31University of Manitoba, Winnipeg, MB, Canada; 2Department of Medicine, Section of Infectious Diseases, Centro de Educación Médica e Investigaciones Clínicas (CEMIC), Buenos Aires, Argentina; 3Theravance, Inc., South San Francisco, CA, USA Background: Hospital-acquired pneumonia (HAP) is the most common health care-associated infection contributing to death. Studies have indicated that there may be differences in the causative pathogens and outcomes of ventilator-associated pneumonia (VAP) and non-ventilator-associated pneumonia (NV-HAP). However, with limited NV-HAP-specific data available, treatment is generally based on data from studies of VAP. The Phase 3 Assessment of Telavancin for Treatment of Hospital-Acquired Pneumonia (ATTAIN) studies were two double-blind randomized controlled trials that demonstrated the non-inferiority of telavancin to vancomycin for treatment of Gram-positive HAP. We conducted a post hoc subgroup analysis of patients enrolled in the ATTAIN studies who had NV-HAP. Methods: Data from the two ATTAIN studies were pooled, and patients with NV-HAP were analyzed. The all-treated (AT) population consisted of all randomized patients who received ≥1 dose of study medication, and the clinically evaluable (CE) population consisted of AT patients who were protocol-adherent or who died on or after study day 3, where death was attributable to the HAP episode under study. The primary endpoint was clinical response (cure, failure, or indeterminate) at the follow-up/test of cure visit, conducted 7–14 days after the end of therapy. Results: A total of 1,076 patients (71.6% of overall ATTAIN AT population) had NV-HAP (533 and 543 patients in the telavancin and vancomycin treatment groups, respectively). Clinical cure rates in the CE population were similar for patients with NV-HAP treated with telavancin and vancomycin (83.1% [201/242] and 84.1% [233/277], respectively). In patients with methicillin-resistant Staphylococcus aureus isolated at baseline, cure rates in the CE population were 74.8% (77/103) for telavancin and 79.3% (96/121) for vancomycin. The incidence of adverse events, serious adverse events, and deaths in patients with NV-HAP was similar whether patients received telavancin or vancomycin. Conclusion: This post hoc subgroup analysis of the ATTAIN studies demonstrated similar cure rates for telavancin and vancomycin for treatment of NV-HAP. Keywords: nosocomial pneumonia, Staphylococcus aureus, methicillin-resistant Staphylococcus aureus

Published
2014

9. Future Aspects

Author

Segev, S., Rubinstein, E., Kuhlmann, J., editor, Dalhoff, A., editor, and Zeiler, H.-J., editor

Published
1998
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12. How IL-2 can affect melanoma cells

Author

Plaisance, S., Alileche, A., Rubinstein, E., Han, D., Azzarone, B., Jasmin, C., Banzet, P., editor, Holland, J. F., editor, Khayat, D., editor, and Weil, M., editor

Published
1994
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15. The Relationship of Pulsatile Cerebrospinal Fluid Flow to Cerebral Blood Flow and Intracranial Pressure: A New Theoretical Model

Author

Bergsneider, Marvin, Alwan, A. A., Falkson, L., Rubinstein, E. H., Reulen, Hans-J., editor, Steiger, H.-J., editor, Marmarou, Anthony, editor, Bullock, Ross, editor, Avezaat, Cees, editor, Baethmann, Alexander, editor, Becker, Donald, editor, Brock, Mario, editor, Hoff, Julian, editor, Nagai, Hajime, editor, and Teasdale, Graham, editor

Published
1998
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22. Candida infective endocarditis

Author

Baddley, J. W., Benjamin, Jr., D. K., Patel, M., Miró, J., Athan, E., Barsic, B., Bouza, E., Clara, L., Elliott, T., Kanafani, Z., Klein, J., Lerakis, S., Levine, D., Spelman, D., Rubinstein, E., Tornos, P., Morris, A. J., Pappas, P., Fowler, Jr., V. G., Chu, V. H., Cabell, C., and The International Collaboration on Endocarditis—Prospective Cohort Study Group (ICE-PCS)

Published
2008
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25. Assessing anti-estrogenic effects of AHR ligands in primary human and rat endometrial epithelial cells

Author

van den Brand, A. D., Rubinstein, E., de Jong, P. C., van den Berg, M., van Duursen, M. B.M., van den Brand, A. D., Rubinstein, E., de Jong, P. C., van den Berg, M., and van Duursen, M. B.M.

Abstract

Unopposed estrogenic action in the uterus can lead to the development of endometrial cancer in both humans and rats. Aryl hydrocarbon receptor (AHR) activation gives rise to anti-estrogenic actions and may consequently reduce the development of endometrial cancer. In this study, the anti-estrogenic potential of the AHR ligands 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and DELAQ, a metabolite of the pharmaceutical laquinimod, was assessed in in primary human and rat endometrial epithelial cells (EECs) with and without co-exposure to endogenous hormones. In human EECs, estradiol and progesterone did not affect AHR gene expression, but in rat EECs, progesterone decreased Ahre xpression (1.4-fold). In accordance, AHR-mediated induction of Cyp1a1/1b1 expression by DELAQ and TCDD decreased in hormone-treated rat EECs. DELAQ was 22-fold more potent than TCDD in human EECs in inducing CYP1A1/1B1 gene expression, while DELAQ was approximately 16−33-fold less potent than TCDD in rat EECs. In human EECs, 10 nM DELAQ decreased estradiol-induced expression of growth-regulated estrogen receptor binding 1 (GREB1) by 1.8-fold. In rat EECs, both DELAQ and TCDD did not affect the expression of estradiol-induced genes. This study shows that AHR ligand DELAQ, but not TCDD, causes anti-estrogenic effects in primary human EECs. Furthermore, although AHR-mediated CYP1A1/1B1/Cyp1a1/1b1 induction by DELAQ and TCDD was stronger in rat EECs than human EECs, this did not result in apparent anti-estrogenic effects in the rat cells. This study shows that primary human and rat endometrial cells respond differently towards hormones and AHR ligands. This should be considered in human risk assessment based on rodent studies.

Published
2020

27. Voriconazole versus a regimen of amphotericin B followed by fluconazole for candidaemia in non-neutropenic patients: a randomised non-inferiority trial

Author

Kullberg, B.J., Sobel, J.D., Ruhnke, M., Pappas, P.G., Viscoli, C., Rex, J.H., Cleary, J.D., Rubinstein, E., Church, L.W.P., Brown, J.M., Schlamm, H.T., Oborska, I.T., Hilton, F., and Hadges, M.R.

Subjects
Amphotericin B -- Dosage and administration, Amphotericin B -- Evaluation, Fluconazole -- Dosage and administration, Fluconazole -- Evaluation, Candidiasis -- Drug therapy
Published
2005

37. GH3 and RC-4BC cell lines are not suitable as in vitro models to study prolactin modulation and AHR responsiveness in rat pituitary

Author

van den Brand, A.D., Rubinstein, E., van den Berg, M., van Duursen, M.B.M., One Health Toxicologie, dIRAS RA-1, E&H: Environmental Health and Toxicology, AIMMS, One Health Toxicologie, and dIRAS RA-1

Subjects
0301 basic medicine, medicine.medical_specialty, endocrine system, Polychlorinated Dibenzodioxins, 030209 endocrinology & metabolism, Biochemistry, Models, Biological, Cell Line, Rats, Sprague-Dawley, 03 medical and health sciences, 0302 clinical medicine, Endocrinology, Quinpirole, SDG 3 - Good Health and Well-being, Internal medicine, Gene expression, medicine, Animals, Secretion, Rats, Wistar, Molecular Biology, Aryl hydrocarbon receptor, biology, Chemistry, Prolactin, Rats, 030104 developmental biology, Pituitary, Receptors, Aryl Hydrocarbon, Dopamine receptor, Cell culture, Pituitary Gland, Uterine Neoplasms, biology.protein, Rat, Female, hormones, hormone substitutes, and hormone antagonists, Hormone, medicine.drug
Abstract

Some environmental contaminants and pharmaceuticals increase the incidence of uterine tumors in toxicological studies with rats. These tumors can result from a hormonal imbalance due to rat-specific disrupted pituitary prolactin regulation, and are therefore of questionable relevance for humans. In this study we compared in vitro prolactin regulation in rat primary pituitary cells to that in pituitary cell lines, GH3 and RC-4BC. Moreover, we assessed the potential effects of aryl hydrocarbon receptor (AHR) activation on prolactin regulation by using two different AHR agonists, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and DELAQ, the N-deethylated minor metabolite of the pharmaceutical laquinimod. In rat primary pituitary cells, known prolactin stimulant thyrotropin-releasing hormone (TRH) marginally increased prolactin secretion (1.2-fold) and gene expression (1.3-fold). In contrast, synthetic dopamine receptor agonist quinpirole, a known inhibitor of prolactin release, significantly inhibited prolactin secretion (2.6-fold) and gene expression (3.6-fold). In GH3 cells, TRH strongly increased prolactin secretion (6.8-fold) and gene expression (30.8-fold), whereas quinpirole did not affect prolactin secretion nor gene expression. In RC-4BC cells, both TRH and quinpirole did not modulate prolactin secretion nor gene expression. Prolactin secretion and gene expression did not significantly change upon exposure to TCDD or DELAQ. However, DELAQ, but not TCDD, attenuated quinpirole-inhibited prolactin gene expression by 51% in primary pituitary cells. This study shows that pituitary prolactin regulation in rat primary pituitary cells in vitro is distinctly different from rat pituitary cell lines GH3 and RC-4BC. Therefore, effects on pituitary prolactin regulation in vitro should best be performed using rat primary pituitary cells. Additionally, AHR ligands may interact with rat pituitary prolactin regulation, but this appears to depend on the ligand and constitutive prolactin secretion. However, interpretation of the in vitro results with respect to occurrence of uterine tumors in rats should take the complex regulation of prolactin release in the pituitary into account as well as the in vivo hypothalamus-pituitary-gonadal (HPG) axis and its feedback loops.

Published
2019

38. Primary endometrial 3D co-cultures: A comparison between human and rat endometrium

Author

van den Brand, A D, Rubinstein, E, de Jong, P C, van den Berg, M, van Duursen, M B M, One Health Toxicologie, dIRAS RA-1, One Health Toxicologie, dIRAS RA-1, E&H: Environmental Health and Toxicology, and AIMMS

Subjects
0301 basic medicine, Polychlorinated Dibenzodioxins, Endocrinology, Diabetes and Metabolism, Clinical Biochemistry, Estrogen receptor, Quinolones, Hormone receptors, Ligands, Endometrium, Biochemistry, Rats, Sprague-Dawley, 0302 clinical medicine, Endocrinology, Gene expression, endometrium, Cells, Cultured, Aryl hydrocarbon receptor, biology, Chemistry, aryl hydrocarbon receptor, medicine.anatomical_structure, Hormone receptor, 030220 oncology & carcinogenesis, Molecular Medicine, Female, cytochrome P450 1A1, medicine.medical_specialty, Cytochrome P450 1A1, 03 medical and health sciences, Aromatase, In vivo, Cell Line, Tumor, Internal medicine, Cytochrome P-450 CYP1A1, medicine, Animals, Humans, Molecular Biology, Estrogen Receptor alpha, hormone receptors, Cytochrome P450, Epithelial Cells, Cell Biology, Coculture Techniques, 030104 developmental biology, Receptors, Aryl Hydrocarbon, biology.protein, Stromal Cells, Hormone
Abstract

Human and rat reproductive systems differ significantly with respect to hormonal cyclicity and endometrial cell behavior. However, species-differences in endometrial cell responses upon hormonal stimulation and exposure to potentially toxic compounds are poorly characterized. In this study, human and rat endometrial hormonal responses were assessed in vitro using a 3D co-culture model of primary human and rat endometrial cells. The models were exposed to the aryl hydrocarbon receptor (AHR) ligands 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), laquinimod, and its AHR active metabolite DELAQ. In both the human and rat endometrial models, estrogen receptor and progesterone receptor gene expression was modulated by the hormonal treatments, comparable to the in vivo situation. AHR gene expression in the human endometrial model did not change when exposed to hormones. In contrast, AHR expression decreased 2-fold in the rat model when exposed to predominantly progesterone, which resulted in a 2.8-fold attenuation of gene expression induction of cytochrome P450 1A1 (CYP1A1) by TCDD. TCDD and DELAQ, but not laquinimod, concentration-dependently induced CYP1A1 gene expression in both human and rat endometrial models. Interestingly, the relative degree of DELAQ to induce CYP1A1 was higher than that of TCDD in the human model, while it was lower in the rat model. These data clearly show species-differences in response to hormones and AHR ligands between human and rat endometrial cells in vitro, which might greatly affect the applicability of the rat as translational model for human endometrial effects. This warrants further development of human relevant, endometrium-specific test methods for risk assessment purposes.

Published
2019

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