Bio

Clinical Focus


  • Pediatric Critical Care Medicine
  • Pediatric Cardiac Intensive Care

Academic Appointments


Professional Education


  • Fellowship:Stanford University School of Medicine (2009) CA
  • Fellowship:Stanford Hospital and Clinics (2008) CA
  • Residency:University of North Carolina (2004) NC
  • Internship:University of North Carolina (2002) NC
  • Medical Education:University of North Carolina School of Medicine (2001) NC
  • Board Certification: Pediatric Critical Care Medicine, American Board of Pediatrics (2008)

Publications

Journal Articles


  • Sedative and analgesic use on night and day shifts in a pediatric cardiovascular intensive care unit. AACN advanced critical care Staveski, S. L., Tesoro, T. M., Cisco, M. J., Roth, S. J., Shin, A. Y. 2014; 25 (2): 114-118

    Abstract

    The use of sedative and analgesic medications is directly linked to patient outcomes. The practice of administering as-needed sedative or analgesic medications deserves further exploration. We hypothesized that important variations exist in the practice of administering as-needed medications in the intensive care unit (ICU). We aimed to determine the influence of time of day on the practice of administering as-needed sedative or analgesic medications to children in the ICU.Medication administration records of patients admitted to our pediatric cardiovascular ICU during a 4-month period were reviewed to determine the frequency and timing of as-needed medication usage by shift.A total of 152 ICU admissions (1854 patient days) were reviewed. A significantly greater number of as-needed doses were administered during the night shift (fentanyl, P = .005; lorazepam, P = .03; midazolam, P = .0003; diphenhydramine, P = .0003; and chloral hydrate, P = .0006). These differences remained statistically significant after excluding doses given during the first 6 hours after cardiovascular surgery. Morphine administration was similar between shifts (P = .08).We identified a pattern of increased administration of as-needed sedative or analgesic medications during nights. Further research is needed to identify the underlying causes of this practice variation.

    View details for DOI 10.1097/NCI.0000000000000023

    View details for PubMedID 24752023

  • Survival after extreme left atrial hypertension and pulmonary hemorrhage in an infant supported with extracorporeal membrane oxygenation for refractory atrial flutter PEDIATRIC CRITICAL CARE MEDICINE Cisco, M. J., Asija, R., Dubin, A. M., Perry, S. B., Hanley, F. L., Roth, S. J. 2011; 12 (3): E149-E152

    Abstract

    We report here the survival of an infant who developed extreme left atrial hypertension and severe pulmonary hemorrhage while supported with extracorporeal membrane oxygenation for refractory atrial flutter. The patient recovered after decompression of the left heart and catheter ablation of the atrioventricular node.Lucile Packard Children's Hospital (Stanford, CA).Chart review.Recovery of lung function is possible despite systemic-level left atrial pressure resulting in pulmonary hemorrhage and complete solidification of lung parenchyma on gross inspection. Resolution of pulmonary hemorrhage despite anticoagulation while on extracorporeal membrane oxygenation can occur after relief of left atrial hypertension.

    View details for DOI 10.1097/PCC.0b013e3181e8b3e5

    View details for Web of Science ID 000290248500008

    View details for PubMedID 20693934

  • A physical map, including a BAC/PAC clone contig, of the Williams-Beuren syndrome-deletion region at 7q11.23 AMERICAN JOURNAL OF HUMAN GENETICS Peoples, R., Franke, Y., Wang, Y. K., Perez-Jurado, L., Paperna, T., Cisco, M., FRANCKE, U. 2000; 66 (1): 47-68

    Abstract

    Williams-Beuren syndrome (WBS) is a developmental disorder caused by haploinsufficiency for genes in a 2-cM region of chromosome band 7q11.23. With the exception of vascular stenoses due to deletion of the elastin gene, the various features of WBS have not yet been attributed to specific genes. Although >/=16 genes have been identified within the WBS deletion, completion of a physical map of the region has been difficult because of the large duplicated regions flanking the deletion. We present a physical map of the WBS deletion and flanking regions, based on assembly of a bacterial artificial chromosome/P1-derived artificial chromosome contig, analysis of high-throughput genome-sequence data, and long-range restriction mapping of genomic and cloned DNA by pulsed-field gel electrophoresis. Our map encompasses 3 Mb, including 1.6 Mb within the deletion. Two large duplicons, flanking the deletion, of >/=320 kb contain unique sequence elements from the internal border regions of the deletion, such as sequences from GTF2I (telomeric) and FKBP6 (centromeric). A third copy of this duplicon exists in inverted orientation distal to the telomeric flanking one. These duplicons show stronger sequence conservation with regard to each other than to the presumptive ancestral loci within the common deletion region. Sequence elements originating from beyond 7q11.23 are also present in these duplicons. Although the duplicons are not present in mice, the order of the single-copy genes in the conserved syntenic region of mouse chromosome 5 is inverted relative to the human map. A model is presented for a mechanism of WBS-deletion formation, based on the orientation of duplicons' components relative to each other and to the ancestral elements within the deletion region.

    View details for Web of Science ID 000085033600007

    View details for PubMedID 10631136

  • Identification of the WBSCR9 gene, encoding a novel transcriptional regulator, in the Williams-Beuren syndrome deletion at 7q11.23 CYTOGENETICS AND CELL GENETICS Peoples, R. J., Cisco, M. J., Kaplan, P., Francke, U. 1998; 82 (3-4): 238-246

    Abstract

    We have identified a novel gene (WBSCR9) within the common Williams-Beuren syndrome (WBS) deletion by interspecies sequence conservation. The WBSCR9 gene encodes a roughly 7-kb transcript with an open reading frame of 1483 amino acids and a predicted protein product size of 170.8 kDa. WBSCR9 is comprised of at least 20 exons extending over 60 kb. The transcript is expressed ubiquitously throughout development and is subject to alternative splicing. Functional motifs identified by sequence homology searches include a bromodomain; a PHD, or C4HC3, finger; several putative nuclear localization signals; four nuclear receptor binding motifs; a polyglutamate stretch and two PEST sequences. Bromodomains, PHD motifs and nuclear receptor binding motifs are cardinal features of proteins that are involved in chromatin remodeling and modulation of transcription. Haploinsufficiency for WBSCR9 gene products may contribute to the complex phenotype of WBS by interacting with tissue-specific regulatory factors during development.

    View details for Web of Science ID 000077796000023

    View details for PubMedID 9858827

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