Kaitlin Flannery

All Publications

• Bradycardia and asystole during temporomandibular joint reconstruction PEDIATRIC ANESTHESIA Flannery, K. M., Yu, J. W., Resnick, C. M., Evans, F. M. 2020; 30 (10): 1146-1148

  Abstract

  Anesthesia providers are familiar with the oculocardiac reflex, one type of trigeminocardiac reflex. While less common, arrhythmias associated with manipulation of other trigeminal nerve branches can occur. We report the presentation and management of bradycardia and asystole from stimulation of the mandibular branch of the trigeminal nerve during temporomandibular joint reconstruction.

  View details for DOI 10.1111/pan.13984

  View details for Web of Science ID 000563616100001

  View details for PubMedID 32741014

• Management of a Pediatric Patient With a Left Ventricular Assist Device and Symptomatic Acquired von Willebrand Syndrome Presenting for Orthotopic Heart Transplant. Seminars in cardiothoracic and vascular anesthesia Flannery, K. M., Kamra, K., Maeda, K., Shuttleworth, P., Almond, C., Navaratnam, M. 2020: 1089253220949386

  Abstract

  We present the successful perioperative management of an 11-year-old patient presenting for heart transplant with a left ventricular assist device, symptomatic acquired von Willebrand syndrome, and recent preoperative intracranial hemorrhage. A brief review of the pathophysiology of acquired von Willebrand syndrome is included. As the number of pediatric patients supported with ventricular assist devices continues to increase, the management of symptomatic acquired von Willebrand syndrome during the perioperative period is an important consideration for anesthesiologists.

  View details for DOI 10.1177/1089253220949386

  View details for PubMedID 32772894

• Perioperative Management of the Pediatric Patient on Medicinal Marijuana: What Anesthesiologists Should Know. Anesthesia and analgesia Flannery, K. M., D'Souza, G. n., Agarwal, R. n. 2019

  Abstract

  In 2018, 29 states allow the use of medicinal marijuana. In these states, minors, with parental permission, are granted access. Use has increased in some states, although there remains a paucity of clear evidence regarding usefulness and dosing. There are 2 Food and Drug Administration-approved synthetic derivatives. One purified compound was just approved by the Food and Drug Administration, and another is undergoing Food and Drug Administration review. This article will review the literature regarding the use of each of these compounds in the literature, with particular attention to data in children. The history, known pharmacology, data from nonmedicinal use, current evidence, and anesthetic considerations will be described.

  View details for DOI 10.1213/ANE.0000000000003956

  View details for PubMedID 30985382

• LMNA variants cause cytoplasmic distribution of nuclear pore proteins in Drosophila and human muscle HUMAN MOLECULAR GENETICS Dialynas, G., Flannery, K. M., Zirbel, L. N., Nagy, P. L., Mathews, K. D., Moore, S. A., Wallrath, L. L. 2012; 21 (7): 1544-1556

  Abstract

  Mutations in the human LMNA gene, encoding A-type lamins, give rise to laminopathies, which include several types of muscular dystrophy. Here, heterozygous sequence variants in LMNA, which result in single amino-acid substitutions, were identified in patients exhibiting muscle weakness. To assess whether the substitutions altered lamin function, we performed in vivo analyses using a Drosophila model. Stocks were generated that expressed mutant forms of the Drosophila A-type lamin modeled after each variant. Larvae were used for motility assays and histochemical staining of the body-wall muscle. In parallel, immunohistochemical analyses were performed on human muscle biopsy samples from the patients. In control flies, muscle-specific expression of the wild-type A-type lamin had no apparent affect. In contrast, expression of the mutant A-type lamins caused dominant larval muscle defects and semi-lethality at the pupal stage. Histochemical staining of larval body wall muscle revealed that the mutant A-type lamin, B-type lamins, the Sad1p, UNC-84 domain protein Klaroid and nuclear pore complex proteins were mislocalized to the cytoplasm. In addition, cytoplasmic actin filaments were disorganized, suggesting links between the nuclear lamina and the cytoskeleton were disrupted. Muscle biopsies from the patients showed dystrophic histopathology and architectural abnormalities similar to the Drosophila larvae, including cytoplasmic distribution of nuclear envelope proteins. These data provide evidence that the Drosophila model can be used to assess the function of novel LMNA mutations and support the idea that loss of cellular compartmentalization of nuclear proteins contributes to muscle disease pathogenesis.

  View details for DOI 10.1093/hmg/ddr592

  View details for Web of Science ID 000301299700009

  View details for PubMedID 22186027

  View details for PubMedCentralID PMC3298278

• Domains of Heterochromatin Protein 1 Required for Drosophila melanogaster Heterochromatin Spreading GENETICS Hines, K. A., Cryderman, D. E., Flannery, K. M., Yang, H., Vitalini, M. W., Hazelrigg, T., Mizzen, C. A., Wallrath, L. L. 2009; 182 (4): 967-977

  Abstract

  Centric regions of eukaryotic genomes are packaged into heterochromatin, which possesses the ability to spread along the chromosome and silence gene expression. The process of spreading has been challenging to study at the molecular level due to repetitious sequences within centric regions. A heterochromatin protein 1 (HP1) tethering system was developed that generates "ectopic heterochromatin" at sites within euchromatic regions of the Drosophila melanogaster genome. Using this system, we show that HP1 dimerization and the PxVxL interaction platform formed by dimerization of the HP1 chromo shadow domain are necessary for spreading to a downstream reporter gene located 3.7 kb away. Surprisingly, either the HP1 chromo domain or the chromo shadow domain alone is sufficient for spreading and silencing at a downstream reporter gene located 1.9 kb away. Spreading is dependent on at least two H3K9 methyltransferases, with SU(VAR)3-9 playing a greater role at the 3.7-kb reporter and dSETDB1 predominately acting at the 1.9 kb reporter. These data support a model whereby HP1 takes part in multiple mechanisms of silencing and spreading.

  View details for DOI 10.1534/genetics.109.105338

  View details for Web of Science ID 000270214000005

  View details for PubMedID 19487560

  View details for PubMedCentralID PMC2728884