Jennifer McNally
Positions:
Assistant Professor of Obstetrics and Gynecology
Obstetrics and Gynecology, Gynecologic Oncology
School of Medicine
Member of the Duke Cancer Institute
Duke Cancer Institute
School of Medicine
Education:
M.D. 2010
Yale University School of Medicine
Residency, Obstetrics And Gynecology
Stanford University
UCSF/Stanford Fellowship in Gynecology Oncology, Obstetrics And Gynecology
University of California San Francisco, School of Medicine
Publications:
The omentum and omentectomy in epithelial ovarian cancer: A reappraisal
Authors
Arie, AB; McNally, L; Kapp, DS; Teng, NNH
MLA Citation
Arie, Alon Ben, et al. “The omentum and omentectomy in epithelial ovarian cancer: A reappraisal.” Gynecologic Oncology, vol. 131, no. 3, Elsevier BV, Dec. 2013, pp. 784–90. Crossref, doi:10.1016/j.ygyno.2013.09.013.
URI
https://scholars.duke.edu/individual/pub1449042
Source
crossref
Published In
Gynecologic Oncology
Volume
131
Published Date
Start Page
784
End Page
790
DOI
10.1016/j.ygyno.2013.09.013
Urachal Duct Carcinoma Complicating Pregnancy
Authors
McNally, L; Osmundson, S; Barth, R; Chueh, J
MLA Citation
McNally, Leah, et al. “Urachal Duct Carcinoma Complicating Pregnancy.” Obstetrics &Amp; Gynecology, vol. 122, no. 2, Ovid Technologies (Wolters Kluwer Health), Aug. 2013, pp. 469–72. Crossref, doi:10.1097/aog.0b013e318292a3ab.
URI
https://scholars.duke.edu/individual/pub1449043
Source
crossref
Published In
Obstetrics and Gynecology
Volume
122
Published Date
Start Page
469
End Page
472
DOI
10.1097/aog.0b013e318292a3ab
Endoproteolytic Cleavage of TUG Protein Regulates GLUT4 Glucose Transporter Translocation
Authors
Bogan, JS; Rubin, BR; Yu, C; Löffler, MG; Orme, CM; Belman, JP; McNally, LJ; Hao, M; Cresswell, JA
MLA Citation
Bogan, Jonathan S., et al. “Endoproteolytic Cleavage of TUG Protein Regulates GLUT4 Glucose Transporter Translocation.” Journal of Biological Chemistry, vol. 287, no. 28, Elsevier BV, July 2012, pp. 23932–47. Crossref, doi:10.1074/jbc.m112.339457.
URI
https://scholars.duke.edu/individual/pub1449044
Source
crossref
Published In
The Journal of Biological Chemistry
Volume
287
Published Date
Start Page
23932
End Page
23947
DOI
10.1074/jbc.m112.339457
Evolution of calcium-carbonate skeletons in the Hydractiniidae.
Biomineralization has mostly been studied in the class Anthozoa (Phylum Cnidaria), but very little is known about the evolution of the calcified skeleton in the class Hydrozoa or about the processes leading to its formation. The evolution of the calcified skeleton is here investigated in the hydrozoan family Hydractiniidae. A phylogenetic analysis of ribosomal, mitochondrial, and nuclear-protein-coding DNA sequences supported two independent origins of the calcified skeleton within the Hydractiniidae and indicates a case of parallel evolution, as suspected in the Anthozoa. Neither of the two origins of skeleton in the Hydractiniidae has led to either speciose or numerically abundant species, in contrast with other skeletonized hydrozoan families. Finally, we show that the origin of calcified skeletons in the Hydractiniidae is significantly correlated with the distribution of species with calcium carbonate granules within a polyp's gastrodermal cells. This suggests that the presence of these granules precedes the origin of a full skeleton.
Authors
Miglietta, MP; McNally, L; Cunningham, CW
MLA Citation
Miglietta, Maria P., et al. “Evolution of calcium-carbonate skeletons in the Hydractiniidae.” Integr Comp Biol, vol. 50, no. 3, Sept. 2010, pp. 428–35. Pubmed, doi:10.1093/icb/icq102.
URI
https://scholars.duke.edu/individual/pub724834
PMID
21558213
Source
pubmed
Published In
Integr Comp Biol
Volume
50
Published Date
Start Page
428
End Page
435
DOI
10.1093/icb/icq102
Inflammation, Glutamate, and Glia in Depression:<i>A Literature Review</i>
<jats:title>ABSTRACT</jats:title><jats:p>Multiple lines of evidence suggest that inflammation and glutamate dysfunction contribute to the pathophysiology of depression. In this review we provide an overview of how these two systems may interact. Excess levels of inflammatory mediators occur in a subgroup of depressed patients. Studies of acute experimental activation of the immune system with endotoxin and of chronic activation during interferon-α treatment show that inflammation can cause depression. Peripheral inflammation leads to microglial activation which could interfere with excitatory amino acid metabolism leading to inappropriate glutamate receptor activation. Loss of astroglia, a feature of depression, upsets the balance of anti- and pro-inflammatory mediators and further impairs the removal of excitatory amino acids. Microglia activated by excess inflammation, astroglial loss, and inappropriate glutamate receptor activation ultimately disrupt the delicate balance of neuroprotective versus neurotoxic effects in the brain, potentially leading to depression.</jats:p>
Authors
McNally, L; Bhagwagar, Z; Hannestad, J
MLA Citation
McNally, Leah, et al. “Inflammation, Glutamate, and Glia in Depression:A Literature Review.” Cns Spectrums, vol. 13, no. 6, Cambridge University Press (CUP), June 2008, pp. 501–10. Crossref, doi:10.1017/s1092852900016734.
URI
https://scholars.duke.edu/individual/pub1449045
Source
crossref
Published In
Cns Spectrums
Volume
13
Published Date
Start Page
501
End Page
510
DOI
10.1017/s1092852900016734

Assistant Professor of Obstetrics and Gynecology
Contact:
225 Acad Adv Ctr, Box 90694, Durham, NC 27708