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To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ajo.2009.07.035 Byline: Keegan S. Johnson, David S. Chu Abstract: To suggest that sub-Tenon triamcinolone acetonide (TA) injections may be a helpful supplement in patients with scleritis. Author Affiliation: Department of Ophthalmology, New Jersey Medical School -- University of Medicine and Dentistry of New Jersey, Newark, New Jersey Article History: Accepted 28 July 2009

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ajo.2008.09.011 Byline: Martin Roesel (a), Christoph Tappeiner (a)(b), Carsten Heinz (a), Joerg M. Koch (a), Arnd Heiligenhaus (a)(c) Abstract: To compare the effect of intravitreal and orbital floor triamcinolone acetonide (TA) on macular edema, visual outcome, and course of postoperative inflammation after cataract surgery in uveitis patients. Author Affiliation: (a) Department of Ophthalmology, St Franziskus-Hospital, Muenster, Germany (b) Department of Ophthalmology, Inselspital, University of Bern, Bern, Switzerland (c) University of Duisburg-Essen, Duisburg, Essen, Germany Article History: Accepted 5 September 2008

Abstract Background: It is unclear whether asthma is over-diagnosed in developed countries, particularly among obese individuals, who may be more likely than nonobese people to experience dyspnea. Methods: We conducted [...]

Byline: Alan H. Jobe, John P. Newnham, Karen E. Willet, Peter Sly, M.Gore Ervin, Cindy Bachurski, Fred Possmayer, Mikko Hallman, Machiko Ikegami Keywords: Compliance; inflammation; lung maturation; respiratory distress syndrome; surfactant Abstract: Objective: We hypothesized that the proinflammatory response to intra-amniotic endotoxin would induce lung maturation in preterm lambs. Study Design: Ewes were randomly assigned to receive 20 mg Escherichia coli endotoxin by intra-amniotic injection, maternal betamethasone (0.5 mg/kg), or sodium chloride solution. Preterm lambs were delivered at 125 days' gestation and underwent ventilation to assess lung function. Lung gas volume, surfactant concentrations, and inflammation were subsequently evaluated, with data analyzed by analysis of variance. Results: Fetal endotoxin exposure 6 days before delivery increased compliance by 59%, increased lung gas volume 2.3-fold, increased concentrations of surfactant lipids, increased surfactant A and B protein levels, and increased messenger ribonucleic acid expressions for surfactant proteins (all P < .01, vs control group). Betamethasone exposure resulted in less consistent effects. White blood cell counts were increased in fetal membranes and lungs after endotoxin exposure, but there was no severe inflammation. Conclusion: A single fetal exposure to endotoxin resulted in large improvements in postnatal lung function and increases in surfactant concentrations after preterm delivery. These effects were qualitatively larger than those achieved with betamethasone. (Am J Obstet Gynecol 2000;182:401-8.) Author Affiliation: Cincinnati, Ohio, Murfreesboro, Tennessee, Perth, Western Australia, Australia, London, Ontario, Canada, and Oulu, Finland From the Division of Pulmonary Biology, Children's Hospital Medical Center,.sup.a the Department of Obstetrics, Women and Infants Research Foundation, University of Western Australia,.sup.b the Division of Clinical Science, TVW Telethon Institute for Child Health Research, University of Western Australia,.sup.c the Department of Biology, Middle Tennessee State University,.sup.d the Department of Obstetrics and Gynecology, University of Western Ontario,.sup.e and the Department of Pediatrics, Oulu University..sup.f Article History: Received 3 March 1999; Revised 25 June 1999; Accepted 31 August 1999 Article Note: (footnote) [star] Supported by grant HD-12714 from the National Institute of Child Health and Human Development and the Women and Infants Research Foundation, Perth, Western Australia, Australia., [star][star] Reprint requests: Alan H. Jobe, MD, PhD, Children's Hospital Medical Center, Division of Pulmonary Biology, 3333 Burnet Ave, Cincinnati, OH 45229-3039.

Byline: William A. Block, Michael L. Draper, James C. Rose, Jeffrey Schwartz Keywords: Fetal development; adrenal gland; steroidogenesis; ovine Abstract: Objective: Adrenal steroidogenesis is important for maturation of fetal organ systems and plays a role in triggering parturition in ovine pregnancies. Studies have suggested a differential increase in baseline cortisol between twin gestations near term. Our aim was to further delineate the mechanisms responsible for the differences between the hypothalamic-pituitary-adrenal axes of twin fetuses in vivo. Study Design: Surgery was performed on pregnant ewes (n = 6) with twin gestations to implant fetal vascular catheters. After recovery but while the subjects were resting, plasma cortisol concentrations were similar in both fetuses. Fetuses received, intravenously, boluses of adrenocorticotropic hormone at 2 doses, and plasma samples were obtained for analysis of the cortisol response. This stimulation by adrenocorticotropic hormone was then repeated in the same fetuses approximately 4 days later, after the increase of resting daily cortisol values in one but not the other fetus. Results: Cortisol responses to adrenocorticotropic hormone before changes in daily resting cortisol concentrations were indistinguishable between twins. However, after separation of daily resting cortisol values, fetuses in group A (elevated resting cortisol concentration) demonstrated a significantly increased response to stimulation by adrenocorticotropic hormone. Conclusion: These results suggest a differential development in response to stimulation by adrenocorticotropic hormone between twin fetuses in vivo as the mechanism responsible for the asynchronous elevation of one twin's resting plasma cortisol concentration. (Am J Obstet Gynecol 1999;181:498-502.) Article History: Received 10 December 1998; Revised 24 February 1999; Accepted 31 March 1999 Article Note: (footnote) [star] From the Department of Obstetrics and Gynecology, the Department of Physiology and Pharmacology, and the Perinatal Research Laboratories, Wake Forest University School of Medicine., [star][star] Supported by National Institutes of Health grant HD11210-20., a Reprint requests: William A. Block, Jr, MD, Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, East Tennessee State University, Johnson City, TN 37614., aa 0002-9378/99 $8.00 + 0 6/1/98995

Byline: Andrew J. Lodge, Paul J. Chai, C.William Daggett, Ross M. Ungerleider, James Jaggers Abstract: Introduction: Cardiopulmonary bypass produces an inflammatory response that can cause significant postoperative pulmonary dysfunction and total body edema. This study evaluates the efficacy of preoperative methylprednisolone administration in limiting this injury in neonates and compares the effect of giving methylprednisolone 8 hours before an operation to the common practice of adding methylprednisolone to the cardiopulmonary bypass circuit prime. Methods: A control group of neonatal pigs (control; n = 6) received no preoperative medication. One experimental group (n = 6) received methylprednisolone sodium succinate (30 mg/kg) both 8 and 1.5 hours before the operation. A second experimental group received no preoperative treatment, but methylprednisolone (30 mg/kg) was added to the cardiopulmonary bypass circuit prime. All animals underwent cardiopulmonary bypass and 45 minutes of deep hypothermic circulatory arrest. Hemodynamic and pulmonary function data were acquired before cardiopulmonary bypass and at 30 and 60 minutes after bypass. Results: In the control group, pulmonary compliance, alveolar-arterial gradient, and pulmonary vascular resistance were significantly impaired after bypass (P < .01 for each by analysis of variance). In the group that received methylprednisolone, compliance (P = .02), alveolar-arterial gradient (P = .0003), pulmonary vascular resistance (P = .007), and extracellular fluid accumulation (P = .003) were significantly better after bypass when compared with the control group. Results for the group that received no preoperative treatment fell between the control group and the group that received methylprednisolone. Conclusions: When given 8 hours and immediately before the operation, methylprednisolone improves pulmonary compliance after bypass, alveolar-arterial gradient, and pulmonary vascular resistance compared with no treatment. The addition of methylprednisolone to the cardiopulmonary bypass circuit prime is beneficial but inferior to preoperative administration. (J Thorac Cardiovasc Surg 1999;117:515-22) Author Affiliation: Department of Surgery, Duke University Medical Center, Durham, NC. Article History: Received 6 April 1998; Revised 9 July 1998; Revised 7 October 1998; Accepted 6 November 1998 Article Note: (footnote) [star] Address for reprints: James Jaggers, MD, Division of Thoracic Surgery, Department of Surgery, Box 3474, Duke University Medical Center, Durham, NC 27710., [star][star] 12/6/95759

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/S0022-5223(99)70331-4 Byline: Andrew J. Lodge, Paul J. Chai, C.William Daggett, Ross M. Ungerleider, James Jaggers Abstract: Introduction: Cardiopulmonary bypass produces an inflammatory response that can cause significant postoperative pulmonary dysfunction and total body edema. This study evaluates the efficacy of preoperative methylprednisolone administration in limiting this injury in neonates and compares the effect of giving methylprednisolone 8 hours before an operation to the common practice of adding methylprednisolone to the cardiopulmonary bypass circuit prime. Methods: A control group of neonatal pigs (control; n = 6) received no preoperative medication. One experimental group (n = 6) received methylprednisolone sodium succinate (30 mg/kg) both 8 and 1.5 hours before the operation. A second experimental group received no preoperative treatment, but methylprednisolone (30 mg/kg) was added to the cardiopulmonary bypass circuit prime. All animals underwent cardiopulmonary bypass and 45 minutes of deep hypothermic circulatory arrest. Hemodynamic and pulmonary function data were acquired before cardiopulmonary bypass and at 30 and 60 minutes after bypass. Results: In the control group, pulmonary compliance, alveolar-arterial gradient, and pulmonary vascular resistance were significantly impaired after bypass (P < .01 for each by analysis of variance). In the group that received methylprednisolone, compliance (P = .02), alveolar-arterial gradient (P = .0003), pulmonary vascular resistance (P = .007), and extracellular fluid accumulation (P = .003) were significantly better after bypass when compared with the control group. Results for the group that received no preoperative treatment fell between the control group and the group that received methylprednisolone. Conclusions: When given 8 hours and immediately before the operation, methylprednisolone improves pulmonary compliance after bypass, alveolar-arterial gradient, and pulmonary vascular resistance compared with no treatment. The addition of methylprednisolone to the cardiopulmonary bypass circuit prime is beneficial but inferior to preoperative administration. (J Thorac Cardiovasc Surg 1999;117:515-22) Author Affiliation: Department of Surgery, Duke University Medical Center, Durham, NC. Article History: Received 6 April 1998; Revised 9 July 1998; Revised 7 October 1998; Accepted 6 November 1998 Article Note: (footnote) [star] Address for reprints: James Jaggers, MD, Division of Thoracic Surgery, Department of Surgery, Box 3474, Duke University Medical Center, Durham, NC 27710., [star][star] 12/6/95759

Byline: Emanuela Marinoni, Claudia Korebrits, Romolo Di Iorio, Ermelando V. Cosmi, John R.G. Challis Keywords: Corticotropin-releasing hormone; pregnancy; placenta; betamethasone Abstract: OBJECTIVE: The objective was to determine the effects of in vivo administration of prenatal betamethasone in patients at 26 to 35 weeks' gestation on corticotropin-releasing hormone concentrations in maternal and fetal plasma and amniotic fluid, and on corticotropin-releasing hormone localization in placenta and fetal membranes. STUDY DESIGN: A total of 49 pregnant women at risk for preterm delivery between 26 and 35 weeks' gestation were studied. Twenty-six patients received betamethasone (12 mg intramuscularly) for stimulation of fetal lung maturity. Cord blood, amniotic fluid, placental tissue, and fetal membranes were obtained from 22 of these patients at delivery by elective cesarean section at 33.8 [+ or -] 2.4 weeks' gestation. In control patients (n = 23) at comparable gestational age, blood samples were taken for hormone analysis (n = 8), and cord blood, amniotic fluid, and tissues were collected at elective cesarean section at 34.1 [+ or -] 2.3 weeks' gestation. Concentrations of corticotropin-releasing hormone, adrenocorticotropic hormone, and cortisol were determined by radioimmunoassay. Localization of tissue immunoreactive corticotropin-releasing hormone was assessed by immunohistochemistry. RESULTS: Betamethasone caused approximately 90% reduction in maternal cortisol and 50% reduction in maternal plasma adrenocorticotropic hormone. In patients at >30 weeks' gestation, there was a significant increase in maternal plasma corticotropin-releasing hormone concentrations after betamethasone; maternal corticotropin-releasing hormone was not altered significantly in untreated patients. Corticotropin-releasing hormone levels were raised in umbilical cord blood by 48 hours and in amniotic fluid 1 week after betamethasone administration. There was increased immunohistochemical staining for corticotropin-releasing hormone in placental syncytiotrophoblast and in fetal membranes of patients treated with betamethasone. CONCLUSIONS: These studies provide the first evidence for in vivo stimulation of plasma corticotropin-releasing hormone, likely of placental origin, by glucocorticoids in third trimester human pregnancy. The results suggest that increases in endogenous cortisol during normal gestation may contribute to placental corticotropin-releasing hormone output and to the rise in maternal plasma corticotropin-releasing hormone concentrations during late pregnancy. (Am J Obstet Gynecol 1998;178:770-8.) Author Affiliation: Rome, Italy, and Toronto, Ontario, Canada Article History: Received 23 June 1997; Revised 2 September 1997; Accepted 9 October 1997 Article Note: (footnote) [star] From the 2nd Department of Obstetrics and Gynecology, University 'La Sapienza,'a and Departments of Physiology and Obstetrics and Gynecology, University of Toronto.b , [star][star] Supported by the Italian National Council of Research (CNR) and The Medical Research Council of Canada., a Reprint requests: Dr. John R.G. Challis, Department of Physiology, Medical Sciences Building, University of Toronto, Toronto, Ontario, Canada M5S 1A8., aa 6/1/86762

Byline: Jeffrey D. Stewart, Christina L. Gonzalez, H.Dix Christensen, William F. Rayburn Keywords: Betamethasone; multidose; dose comparison; growth; development; mouse Abstract: Objective: Our purpose was to determine in a randomized, placebo-controlled manner whether multiple antenatal doses of betamethasone affect long-term growth and development of exposed mouse offspring. Study Design: Sixty pregnant CD-1 mice received either two, four, or eight antepartum doses of 0.1 mg betamethasone or placebo. Perinatal outcomes, growth, and development of the offspring were compared in a blinded manner. Variables were compared by analysis of variance or I.sup.2 testing. Results: Betamethasone-exposed subjects gained less weight during pregnancy and were delivered of fewer live pups, with fewer male survivors and lower birth weights. These trends were dose related. Growth measurements were similar after the neonatal period. No differences in functional development and physical maturation in the offspring were noted. The reproductive capability, perinatal outcomes, and growth and development of the second-generation offspring were unaffected by betamethasone exposure. Conclusion: Multiple antenatal dosings of betamethasone, reaching toxic levels, did not have an impact on the long-term growth and development of the surviving mouse offspring. Author Affiliation: Oklahoma City, Oklahoma Article Note: (footnote) [star] From the Section of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology,a and the Department of Pharmacology and Toxicology,b University of Oklahoma Health Sciences Center., [star][star] Supported by the J.W. Records Perinatal Research Fund., a Reprint requests: Jeffrey D. Stewart, MD, University of Oklahoma Health Science Center, Department of Obstetrics and Gynecology, Section of Maternal-Fetal Medicine, P.O. Box 26901, 4SP710, Oklahoma City, OK 73190., aa 0002-9378/97 $5.00 + 0 6/6/84564

Byline: Gary E. Hill, Anselmo Alonso, John R. Spurzem, Alfred H. Stammers, Richard A. Robbins Abstract: Cardiopulmonary bypass induces an inflammatory state characterized by tumor necrosis factor-[alpha] release. Integrin CD11b is a neutrophil surface adhesive glycoprotein integrin that is rapidly and permanently unregulated by tumor necrosis factor-[alpha] exposure. The CD11b integrin is known to be the primary neutrophil integrin responsible for neutrophil lung and myocardial entrapment after cardiopulmonary bypass and subsequent reperfusion injury. Twenty-four adults admitted to the hospital for myocardial revascularization were equally randomized to one of three groups: group A (control), group B (methylprednisolone before cardiopulmonary bypass), and group C (low-dose aprotinin protocol). Blood was collected at three times: (1) baseline, (2) 50 minutes of cardiopulmonary bypass duration, and (3) 30 minutes after cardiopulmonary bypass termination. Neutrophil CD11b integrin expression was measured by fluorescence-activated cell sorter analysis and plasma tumor necrosis factor-[alpha]levels measured by enzyme-linked immunosorbent assay. Group A demonstrated significant (p < 0.05) increases in CD11b expression at times 2 and 3 when results were compared with those of the same group baseline and with those of groups B and C at similar times. No significant changes were noted between groups B and C at any time. Group A demonstrated a significant (p < 0.05) increase in levels of tumor necrosis factor-[alpha] at time 3 when results were compared with those of the same group baseline and of groups B and C at the same time. No significant changes were noted between groups B and C at any time. These results demonstrate low-dose aprotinin has a similar antiinflammatory effect to that of methylprednisolone in blunting cardiopulmonary bypass-induced systemic tumor necrosis factor-[alpha] release and neutrophil integrin CD11b upregulation. (J THORAC CARDIOVASC SURG 1995;110:1658-62) Author Affiliation: Omaha, Neb Article History: Received 28 February 1995; Accepted 6 April 1995 Article Note: (footnote) [star] From the Departments of Internal Medicine,b Anesthesiology, a Surgery, c and Perfusion Sciences Education, d University of Nebraska Medical Center, Omaha, Neb., [star][star] Address for reprints: Gary E. Hill, MD, FCCM, Department of Anesthesiology and Internal Medicine, University of Nebraska Medical Center, 600 S. 42 St., Box 984455, Omaha, NE 68198-4455., a 0022-5223/95 $5.00 + 0, aa 12/1/65323

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ajog.2009.09.033 Byline: Matthias Loehle (a), Matthias Schwab (a), Susan Kadner (b), Kristal M. Maner (c), Jeffrey S. Gilbert (d), J. Thomas Brenna (c), Stephen P. Ford (e), Peter W. Nathanielsz (d), Mark J. Nijland (d) Keywords: antenatal glucocorticoids; glucocorticoid formulation; lung maturation Abstract: Glucocorticoid administration to women in preterm labor improves neonatal mortality and morbidity. Fetal exposure to glucocorticoid levels higher than those appropriate to the current gestational stage has multiple organ system effects. Some, eg, fetal hypertension, are maximal at lower than the clinical dose. We hypothesized that the clinical dose has supramaximal lung maturational effects. Author Affiliation: (a) Department of Neurology, University of Jena, Jena, Germany (b) Department of Obstetrics and Gynecology, New York University School of Medicine, New York, NY (c) Division of Nutritional Sciences, Cornell University, Ithaca, NY (d) Department of Obstetrics and Gynecology, University of Texas Health Science Center at San Antonio, San Antonio, TX (e) Department of Animal Science, University of Wyoming, Laramie, WY Article History: Received 14 January 2009; Revised 11 June 2009; Accepted 28 September 2009 Article Note: (footnote) This study was supported by Grant NIH Heart Lung Blood Institute 068649, NHLBI, NIH, HHS., Reprints not available from the authors., Cite this article as: Loehle M, Schwab M, Kadner S, et al. Dose-response effects of betamethasone on maturation of the fetal sheep lung. Am J Obstet Gynecol 2010;202:186.e1-7.

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ajo.2008.12.006 Byline: Ian L. McAllister, Sarojini Vijayasekaran, Simon D. Chen, Dao-Yi Yu Abstract: To investigate the molecular mechanism by which triamcinolone acetonide (TA) may reduce edema in a porcine model of branch retinal vein occlusion (BRVO). Author Affiliation: Lions Eye Institute, Centre for Ophthalmology and Visual Science, The University of Western Australia, Perth, Australia Article History: Accepted 3 December 2008

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