Surgeon
7 years of experience
Video profile
Accepting new patients
225 Newtown Rd
2nd Floor
Warminster, PA 18974
215-441-6800
Locations and availability (2)

Education ?

Medical School Score
University of Illinois at Chicago (2003)
  • Currently 2 of 4 apples
Residency
Hosp. of the Univ. of Pennsy. (2010) *
Surgery
University of Pennsylvania (2010) *
Surgery
Fellowship
Massachusetts General Hospital (2008) *
Medical College of Wisconsin (2011) *
* This information was reported to Vitals by the doctor or doctor's office.

Awards & Distinctions ?

Associations
American College of Surgeons
American Board of Surgery
American Medical Association
American Society for Metabolic and Bariatric Surgery
Society of American Gastrointestinal and Endoscopic Surgeons
Ethicon (bariatric Surgery) (bariatricedge.com)

Affiliations ?

Dr. Noonan is affiliated with 3 hospitals.

Hospital Affilations

Score

Rankings

  • Warminster Hospital
    225 Newtown Rd, Warminster, PA 18974
    • Currently 2 of 4 crosses
  • Abington Memorial Hospital
    1200 Old York Rd, Abington, PA 19001
    • Currently 2 of 4 crosses
  • Abington Memorial Hospital *
  • Publications & Research

    Dr. Noonan has contributed to 7 publications.
    Title Characterization of the Chromosome 1q41q42.12 Region, and the Candidate Gene Disp1, in Patients with Cdh.
    Date November 2010
    Journal American Journal of Medical Genetics. Part A
    Excerpt

    Cytogenetic and molecular cytogenetic studies demonstrate association between congenital diaphragmatic hernia (CDH) and chromosome 1q41q42 deletions. In this study, we screened a large CDH cohort (N=179) for microdeletions in this interval by the multiplex ligation-dependent probe amplification (MLPA) technique, and also sequenced two candidate genes located therein, dispatched 1 (DISP1) and homo sapiens H2.0-like homeobox (HLX). MLPA analysis verified deletions of this region in two cases, an unreported patient with a 46,XY,del(1)(q41q42.13) karyotype and a previously reported patient with a Fryns syndrome phenotype [Kantarci et al., 2006]. HLX sequencing showed a novel but maternally inherited single nucleotide variant (c.27C>G) in a patient with isolated CDH, while DISP1 sequencing revealed a mosaic de novo heterozygous substitution (c.4412C>G; p.Ala1471Gly) in a male with a left-sided Bochdalek hernia plus multiple other anomalies. Pyrosequencing demonstrated the mutant allele was present in 43%, 12%, and 4.5% of the patient's lymphoblastoid, peripheral blood lymphocytes, and saliva cells, respectively. We examined Disp1 expression at day E11.5 of mouse diaphragm formation and confirmed its presence in the pleuroperitoneal fold, as well as the nearby lung which also expresses Sonic hedgehog (Shh). Our report describes the first de novo DISP1 point mutation in a patient with complex CDH. Combining this finding with Disp1 embryonic mouse diaphragm and lung tissue expression, as well as previously reported human chromosome 1q41q42 aberrations in patients with CDH, suggests that DISP1 may warrant further consideration as a CDH candidate gene.

    Title Genetic Tools and Algorithms for Gene Discovery in Major Congenital Anomalies.
    Date February 2009
    Journal Birth Defects Research. Part A, Clinical and Molecular Teratology
    Title Donnai-barrow Syndrome (dbs/foar) in a Child with a Homozygous Lrp2 Mutation Due to Complete Chromosome 2 Paternal Isodisomy.
    Date August 2008
    Journal American Journal of Medical Genetics. Part A
    Excerpt

    Donnai-Barrow syndrome [Faciooculoacousticorenal (FOAR) syndrome; DBS/FOAR] is a rare autosomal recessive disorder resulting from mutations in the LRP2 gene located on chromosome 2q31.1. We report a unique DBS/FOAR patient homozygous for a 4-bp LRP2 deletion secondary to paternal uniparental isodisomy for chromosome 2. The propositus inherited the mutation from his heterozygous carrier father, whereas the mother carried only wild-type LRP2 alleles. This is the first case of DBS/FOAR resulting from uniparental disomy (UPD) and the fourth published case of any paternal UPD 2 ascertained through unmasking of an autosomal recessive disorder. The absence of clinical symptoms above and beyond the classical phenotype in this and the other disorders suggests that paternal chromosome 2 is unlikely to contain imprinted genes notably affecting either growth or development. This report highlights the importance of parental genotyping in order to give accurate genetic counseling for autosomal recessive disorders.

    Title Negative Regulation of the Sh2-homology Containing Protein-tyrosine Phosphatase-1 (shp-1) P2 Promoter by the Htlv-1 Tax Oncoprotein.
    Date October 2007
    Journal Blood
    Excerpt

    Expression of SH(2)-homology-containing protein-tyrosine phosphatase-1 (SHP-1), a candidate tumor suppressor, is repressed in human T-cell leukemia virus type-1 (HTLV-1)-transformed lymphocyte cell lines, adult T-cell leukemia (ATL) cells, and in other hematologic malignancies. However, the mechanisms underlying regulation and repression of SHP-1 remain unclear. Herein, we cloned the putative full-length, hematopoietic cell-specific SHP-1 P2 promoter and identified the "core" promoter regions. HTLV-1 Tax profoundly represses P2 promoter activity and histone deacetylase-1 (HDAC1) potentiates such inhibition. NF-kappaB was implicated as both a rate-limiting factor for basal P2 promoter activity and important for Tax-induced promoter silencing (TIPS). Chromatin immunoprecipitation studies demonstrated that NF-kappaB dissociates from the SHP-1 P2 promoter following the binding of Tax and HDAC1. This is in agreement with coimmunoprecipitation studies where NF-kappaB competed with HDAC1 for association with Tax protein. We propose that in TIPS, Tax recruits HDAC1 to the SHP-1 P2 promoter and forms an inhibitory complex that results in deacetylation and dissociation of NF-kappaB from the promoter and attenuation of SHP-1 expression. TIPS provides a possible first step toward HTLV-1 leukemogenesis through its down-modulation of this key immediate early negative regulator of IL-2 signaling.

    Title Mutations in Lrp2, Which Encodes the Multiligand Receptor Megalin, Cause Donnai-barrow and Facio-oculo-acoustico-renal Syndromes.
    Date September 2007
    Journal Nature Genetics
    Excerpt

    Donnai-Barrow syndrome is associated with agenesis of the corpus callosum, congenital diaphragmatic hernia, facial dysmorphology, ocular anomalies, sensorineural hearing loss and developmental delay. By studying multiplex families, we mapped this disorder to chromosome 2q23.3-31.1 and identified LRP2 mutations in six families with Donnai-Barrow syndrome and one family with facio-oculo-acoustico-renal syndrome. LRP2 encodes megalin, a multiligand uptake receptor that regulates levels of diverse circulating compounds. This work implicates a pathway with potential pharmacological therapeutic targets.

    Title Herpes Zoster During Varicella.
    Date March 2002
    Journal The Pediatric Infectious Disease Journal
    Title Sex Ratio of Parental Investment in Colonies of the Social Wasp Polistes Fuscatus.
    Date
    Journal Science (new York, N.y.)
    Excerpt

    Field estimates of parental investment in the two sexes in the social paper wasp Polistes fuscatus indicate that the mother's interests, rather than those of her worker offspring, are realized. Local competition for mates seemed to be absent, and the population investment ratio was not significantly different from 1:1. Workers are not more closely related to the brood they tend than they would be to their own offspring. The 3/4 relationship between sisters in haplodiploid species cannot account for the maintenance of eusociality in this case.


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