Objectives: To address the clinical significance of sinusoidal heart rate (SHR) pattern and review its occurrence, define its characteristics, and explain its physiopathology. Background: In 1972, Manseau et al. and Kubli et al. described an undulating wave form alternating with a flat or smooth baseline fetal heart rate (FHR) in severely affected, Rh-sensitized and dying fetuses. This FHR pattern was called 'sinusoidal' because of its sine waveform. Subsequently, Modanlou et al. described SHR pattern associated with fetal to maternal hemorrhage causing severe fetal anemia and hydrops fetalis. Both Manseau et al. and Kubli et al. stated that this particular FHR pattern, whatever its pathogenesis, was an extremely significant finding that implied severe fetal jeopardy and impending fetal death. Underlating FHR pattern: Undulating FHR pattern may be due to the following: (1) true SHR pattern; (2) drugs; (3) pre-mortem FHR pattern; (4) pseudo-SHR pattern; and (5) equivocal FHR patterns. Fetal conditions associated with SHR pattern: SHR pattern has been reported with the following fetal conditions: (1) severe fetal anemia of several etiologies; (2) effects of drugs, particularly narcotics; (3) fetal asphyxia/hypoxia; (4) fetal infection; (5) fetal cardiac anomalies; (6) fetal sleep cycles; and (7) sucking and rhythmic movements of fetal mouth. Definition of true SHR pattern: Modanlou and Freeman proposed the following definition for the interpretation of true SHR pattern: (a) stable baseline FHR of 120-160 bpm; (b) amplitude of 5-15 bpm, rarely greater; (c) frequency of 2-5 cycles per minute; (d) fixed or flat short-term variability; (e) oscillation of the sinusoidal wave from above and below a baseline; and (f) no areas of normal FHR variability or reactivity. Physiopathology: Since its early recognition, the physiopathology of SHR became a matter of debate. Murata et al. noted a rise of arginine vasopressin levels in the blood of posthemorrhagic/anemic fetal lamb. Further works by the same authors revealed that with chemical or surgical vagotomy, arginine vasopressin infusion produced SHR pattern, thus providing the role of autonomic nervous system dysfunction combined with the increase in arginine vasopressin as the etiology. Conclusion: SHR is a rare occurrence. A true SHR is an ominous sign of fetal jeopardy needing immediate intervention. The correct diagnosis of true SHR pattern should also include fetal biophysical profile and the absence of drugs such as narcotics.

Objective: We examined the hypothesis that a single course of antenatal betamethasone influences the maternal-fetal insulin-IGF-GH axis. Design: A prospective, observational, pilot study consisting of four groups of pregnant women: (1) received betamethasone and delivered 2 weeks post treatment; (III) untreated women who delivered 37 weeks (term controls). Maternal and mixed umbilical cord blood was collected at delivery and analyzed for insulin, glucose, IGF-I IGF-II, IGFBP-1, IGFBP-3, GH and GHBP. Results: Betamethasone increased maternal insulin, glucose and IGF-I levels without affecting IGFBPs. In the fetal compartment, betamethasone treatment was associated with a delayed suppressive effect on GH and a sustained suppressive effect on IGF-II levels. There were no differences in infant size or neonatal morbidities between patients who delivered 2 weeks post betamethasone treatment. In Group IV, birth weight correlated positively with cord IGF-I levels (r(2) = 0.41, p = 0.0098) and negatively with cord IGFBP-1 levels (r(2) = 0.51, p = 0.0039), and ponderal index correlated negatively with cord IGFBP-1 levels (r(2) = 0.27, p < 0.05). Conclusions: A single course of antenatal betamethasone influences the maternal-fetal insulin-IGF-GH axis, particularly fetal TGF-II levels, without measurable anthropornetric changes at birth. Whether these effects have implications beyond the neonatal period remains to be determined. (c) 2006 Elsevier Ltd. All rights reserved.

Editors: Eric Hegedus, Thanh Truong

Faculty Advisors: Johanna Shapiro, Ph.D.; Lloyd Rucker, M.D.

Thank you to Dean Thomas Cesario and to the following offices that helped support and distribute Plexus:  Office of Medical Education, Office of Alumni Relations, and the Office of Admissions and Outreach

Printed by Graphic Depot

Plexus 2002 UCI College of Medicine

Editors:  Thomas King, Gráinne McEvoy

Faculty Advisors:  Johanna Shapiro, Lloyd Rucker

Our sincere thanks to the following people and departments:

Kate Aceves, for typesetting, design & production, without whom we’d probably still be struggling with putting this together!

All our contributors for their creativity and generosity with their work

Publication of this journal is supported by funds from USPHS UCI Grant for the Establishment of Departments of Family Medicine No. PE10152, whom we thank for their generous funding of this fledgling effort.

UCI College of Medicine Journal of Arts & Humanities 2000 Edition Volume 1

PLEXUS 2000 UCI College of Medicine

Editor-in-Chief:  Gráinne McEvoy-Mulholland

Managing Editor: Thomas Kang

Editorial Board: Marisa Chang, Jade Jena, Lisa Lim, Susan Lin, Thanh Truong, Ranjii Vargheses Faculty Advisors: Johanna Shapiro, Ph.D.; Lloyd Rucker, M.D.

Thank you again this year to Kate Aceves for typesetting, design and production. We are so grateful for her generosity with her time and skills.

Thank you to Dean Thomas Cesario for his support of our endeavor and for funding copies of Plexus for distribution to the UCI College of Medicine community.

Thank you to all of the departments and individuals who chose to support and distribute Plexus – Dr. Manetta & Medical Education, Maureen Hausen & Alumni, Dr. Scherger & Family Medicine, Gayle Pierce & Peggy Harvey-Lee and Admissions, and of course, our individual benefactors Dr. Johanna Shapiro and Tom’s dad.

Thank you to Mark Mulholland for doing lots of baby care while Gráinne worked on Plexus, and to Aidan Mulholland for being so patient with his mom.