Danwei Wu

All Publications

• High-dimensional, targeted immunogenetic profiles of "idiopathic" myelitis with correlative risk and protective factors Sarkar, T., Sumera, J., Tomczak, A., Bachar, S., Ton-Nu, C., Joseph, Y., Lee, J., Osoegawa, K., Vina, M., Wu, D., Nie, E., Sattarnezhad, N., McDonald, J., Galetta, K., Kipp, L., Van Haren, K., Dunn, J., Han, M., Lock, C. SAGE PUBLICATIONS LTD. 2024: 1230-1231

  View details for Web of Science ID 001324906903494

• Paired serum and CSF immunoprofiling guides treatment of refractory CNS autoimmunity Wu, D., Sarkar, T., Nie, E., Galetta, K., McDonald, J., Tomczak, A., Sumera, J., Kipp, L., Lock, C., Dunn, J., Han, M. SAGE PUBLICATIONS LTD. 2024: 1196

  View details for Web of Science ID 001324906903445

• Myeloid cell replacement is neuroprotective in chronic experimental autoimmune encephalomyelitis. Nature neuroscience Mader, M. M., Napole, A., Wu, D., Atkins, M., Scavetti, A., Shibuya, Y., Foltz, A., Hahn, O., Yoo, Y., Danziger, R., Tan, C., Wyss-Coray, T., Steinman, L., Wernig, M. 2024

  Abstract

  Multiple sclerosis (MS) is an autoimmune disease characterized by demyelination of the central nervous system (CNS). Autologous hematopoietic cell transplantation (HCT) shows promising benefits for relapsing-remitting MS in open-label clinical studies, but the cellular mechanisms underlying its therapeutic effects remain unclear. Using single-nucleus RNA sequencing, we identify a reactive myeloid cell state in chronic experimental autoimmune encephalitis (EAE) associated with neuroprotection and immune suppression. HCT in EAE mice results in an increase of the neuroprotective myeloid state, improvement of neurological deficits, reduced number of demyelinated lesions, decreased number of effector Tcells and amelioration of reactive astrogliosis. Enhancing myeloid cell incorporation after a modified HCT further improved these neuroprotective effects. These data suggest that myeloid cell manipulation or replacement may be an effective therapeutic strategy for chronic inflammatory conditions of the CNS.

  View details for DOI 10.1038/s41593-024-01609-3

  View details for PubMedID 38514857

• Risk of acute stroke in young patients with new-onset lupus nephritis: a case series Wu, D., Han, M., Lee, S. LIPPINCOTT WILLIAMS & WILKINS. 2023

  View details for DOI 10.1212/WNL.0000000000204219

  View details for Web of Science ID 001053672106241

• ANK2 autism mutation targeting giant ankyrin-B promotes axon branching and ectopic connectivity PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Yang, R., Walder-Christensen, K. K., Kim, N., Wu, D., Lorenzo, D. N., Badea, A., Jiang, Y., Yin, H. H., Wetsel, W. C., Bennett, V. 2019; 116 (30): 15262-15271

  Abstract

  Giant ankyrin-B (ankB) is a neurospecific alternatively spliced variant of ANK2, a high-confidence autism spectrum disorder (ASD) gene. We report that a mouse model for human ASD mutation of giant ankB exhibits increased axonal branching in cultured neurons with ectopic CNS axon connectivity, as well as with a transient increase in excitatory synapses during postnatal development. We elucidate a mechanism normally limiting axon branching, whereby giant ankB localizes to periodic axonal plasma membrane domains through L1 cell-adhesion molecule protein, where it couples microtubules to the plasma membrane and prevents microtubule entry into nascent axon branches. Giant ankB mutation or deficiency results in a dominantly inherited impairment in selected communicative and social behaviors combined with superior executive function. Thus, gain of axon branching due to giant ankB-deficiency/mutation is a candidate cellular mechanism to explain aberrant structural connectivity and penetrant behavioral consequences in mice as well as humans bearing ASD-related ANK2 mutations.

  View details for DOI 10.1073/pnas.1904348116

  View details for Web of Science ID 000476715500071

  View details for PubMedID 31285321

  View details for PubMedCentralID PMC6660793

• A Case of Paraneoplastic Guillain-Barré Syndrome Associated with Squamous Cell Carcinoma of the Lung. Cureus Wu, D., Liu, A., Baldinger, E., Frontera, A. T. 2018; 10 (8): e3202

  Abstract

  We report a case of a 61-year-old man with a history of squamous cell carcinoma of the lung presenting with rapidly progressive symmetric ascending weakness with areflexia. The weakness was quickly followed by respiratory decompensation requiring intubation. Lumbar puncture yielded cerebrospinal fluid with elevated protein (177 mg/dL), normal glucose (61 mg/dL), normal red blood cell count (0 per/µl), and normal white blood cell count (0 per/µL). Emergent magnetic resonance imaging of cervical, thoracic, and lumbar spine did not show evidence of metastatic disease, fracture, subluxation, or other causes of cord compression. The patient was diagnosed with acute inflammatory polyneuropathy, also known as Guillain-Barré syndrome. Despite treatment with a five-day course of intravenous immunoglobulin and a subsequent five-day course of plasmapheresis, the patient did not recover respiratory function and died 48 days after diagnosis. To our knowledge, this is the first documented case of Guillain-Barré occurring concomitantly with squamous cell carcinoma of the lung.

  View details for DOI 10.7759/cureus.3202

  View details for PubMedID 30405981

  View details for PubMedCentralID PMC6205880

• The Impact of Breastfeeding on Health Outcomes for Infants Diagnosed with Neonatal Abstinence Syndrome: A Review. Cureus Wu, D., Carre, C. 2018; 10 (7): e3061

  Abstract

  Neonatal abstinence syndrome (NAS) is a neurologic condition resulting from prenatal exposure to opioids. The sudden cessation of opioids in neonates can lead to withdrawal symptoms affecting the neurologic, respiratory, and gastrointestinal systems. Rising opioid use in the United States has led to an increased incidence of infants born with NAS. Despite the growing incidence of NAS, there is a lack of standardized guidelines for intervention and management. Recent studies suggest that non-pharmacological methods should be used as first-line interventions for the reduction of NAS symptoms. Of the non-pharmacological methods, growing literature suggests that breastfeeding may have the potential to reduce symptom severity and improve outcomes. We searched the PubMed and Medline databases for experimental/quasi-experimental studies published from 1997-2018 regarding outcomes in breastfed versus formula-fed neonates with prenatal exposure to opioids. Seven retrospective studies fulfilling the inclusion criteria were reviewed. Collectively, the studies show a strong correlation between breastfeeding and a reduced length of hospital stay, a decreased severity of NAS presentation, and a decreased necessity of pharmacological interventions in infants diagnosed with NAS. From these findings, we recommend breastfeeding as an integral component of the early management of NAS.

  View details for DOI 10.7759/cureus.3061

  View details for PubMedID 30397566

  View details for PubMedCentralID PMC6211775

• Rbm8a Haploinsufficiency Disrupts Embryonic Cortical Development Resulting in Microcephaly JOURNAL OF NEUROSCIENCE Mao, H., Pilaz, L., McMahon, J. J., Golzio, C., Wu, D., Shi, L., Katsanis, N., Silver, D. L. 2015; 35 (18): 7003-7018

  Abstract

  The cerebral cortex is built during embryonic neurogenesis, a period when excitatory neurons are generated from progenitors. Defects in neurogenesis can cause acute neurodevelopmental disorders, such as microcephaly (reduced brain size). Altered dosage of the 1q21.1 locus has been implicated in the etiology of neurodevelopmental phenotypes; however, the role of 1q21.1 genes in neurogenesis has remained elusive. Here, we show that haploinsufficiency for Rbm8a, an exon junction complex (EJC) component within 1q21.1, causes severe microcephaly and defective neurogenesis in the mouse. At the onset of neurogenesis, Rbm8a regulates radial glia proliferation and prevents premature neuronal differentiation. Reduced Rbm8a levels result in subsequent apoptosis of neurons, and to a lesser extent, radial glia. Hence, compared to control, Rbm8a-haploinsufficient brains have fewer progenitors and neurons, resulting in defective cortical lamination. To determine whether reciprocal dosage change of Rbm8a alters embryonic neurogenesis, we overexpressed human RBM8A in two animal models. Using in utero electroporation of mouse neocortices as well as zebrafish models, we find RBM8A overexpression does not significantly perturb progenitor number or head size. Our findings demonstrate that Rbm8a is an essential neurogenesis regulator, and add to a growing literature highlighting roles for EJC components in cortical development and neurodevelopmental pathology. Our results indicate that disruption of RBM8A may contribute to neurodevelopmental phenotypes associated with proximal 1q21.1 microdeletions.

  View details for DOI 10.1523/JNEUROSCI.0018-15.2015

  View details for Web of Science ID 000356668400004

  View details for PubMedID 25948253

  View details for PubMedCentralID PMC4420776