Chester W. Brown

Dr. Chester W. Brown

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Academic Career Length

16Years (2011-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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3 November 2021 in The FASEB Journal
Verified
Journal Article
Closed access
PDF file
RKRoshan Kumari
Roshan Kumari
MIMaria Johnson Irudayam
Maria Johnson Irudayam
QAQusai Al Abdallah
Qusai Al Abdallah
TJTamekia L. Jones
Tamekia L. Jones
TMTahliyah S. Mims
Tahliyah S. Mims
CBChester W. Brown
Chester W. Brown
19 March 2021 in npj Genomic Medicine
Verified
Journal Article
Open access
PDF file
SMSavannah Mwesigwa
Savannah Mwesigwa
LWLesedi Williams
Lesedi Williams
GRGaone Retshabile
Gaone Retshabile
EKEric Katagirya
Eric Katagirya
Gerald MboowaGerald Mboowa
Gerald Mboowa
NHNeil A. Hanchard
Neil A. Hanchard
Human immunodeficiency virus (HIV) infection remains a significant public health burden globally. The role of viral co-infection in the rate of progression of HIV infection has been suggested but not empirically tested, particularly among children. We extracted and classified 42 viral species from whole-exome sequencing (WES) data of 813 HIV-infected children in Botswana and Uganda categorised as either long-term non-progressors (LTNPs) or rapid progressors (RPs). The Ugandan participants had a higher viral community diversity index compared to Batswana (p = 4.6 × 10−13), and viral sequences were more frequently detected among LTNPs than RPs (24% vs 16%;p = 0.008; OR, 1.9; 95% CI, 1.6–2.3), withAnelloviridaeshowing strong association with LTNP status (p = 3 × 10−4;q = 0.004, OR, 3.99; 95% CI, 1.74–10.25). This trend was still evident when stratified by country, sex, and sequencing platform, and after a logistic regression analysis adjusting for age, sex, country, and the sequencing platform (p = 0.02;q = 0.03; OR, 7.3; 95% CI, 1.6–40.5). Torque teno virus (TTV), which made up 95% of theAnelloviridaereads, has been associated with reduced immune activation. We identify an association between viral co-infection and prolonged AIDs-free survival status that may have utility as a biomarker of LTNP and could provide mechanistic insights to HIV progression in children, demonstrating the added value of interrogating off-target WES reads in cohort studies.
15 February 2024 in Brain Sciences
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Journal Article
Open access
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ABAnneliesse A Braden
Anneliesse A Braden
JXJianfeng Xiao
Jianfeng Xiao
RHRoderick Hori
Roderick Hori
CBChester W. Brown
Chester W. Brown
MKMohammad Moshahid Khan
Mohammad Moshahid Khan
Recently, a recurrent de novo dominant mutation in UBTF (c.628G>A, p.Glu210Lys; UBTF E210K) was identified as the cause of a neurological disorder which has been named UBTF Neuroregression Syndrome (UNS), or Childhood-Onset Neurodegeneration with Brain Atrophy (CONDBA). To date, only 17 cases have been reported worldwide. The molecular etiology is a pathogenic variant, E210K, within the HMG-box 2 of Upstream Binding Transcription Factor (UBTF). UBTF, a nucleolar protein, plays an important role in ribosomal RNA (rRNA) synthesis, nucleolar integrity, and cell survival. This variant causes unstable preinitiation complexes to form, resulting in altered rDNA chromatin structures, rRNA dysregulation, DNA damage, and ultimately, neurodegeneration. Defining clinical characteristics of the disorder include but are not limited to developmental regression beginning at approximately three years of age, progressive motor dysfunction, declining cognition, ambulatory loss, and behavioral problems. Histological and neuroimaging abnormalities include cortical atrophy, white matter deficits, and enlarged ventricles. Herein, we present a detailed overview of all published cases as well as the functional roles of UBTF to better understand the pathophysiology. Bringing undiagnosed cases to the attention of clinicians and researchers by making them aware of the clinical features will improve research and support the development of therapeutic interventions.
1 May 2020 in ICSID Review
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Journal Article
Closed access
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CBChester W. Brown
Chester W. Brown
PSPatrick Still
Patrick Still
A problem that arises from time to time in international arbitration proceedings is how an arbitral tribunal is to deal with the evidence of a non-appearing witness. The applicable rules of arbitration typically confirm that the tribunal has the authority to determine (e.g.) the “admissibility, relevance, materiality and weight of the evidence offered,” but they rarely go any further than this. The purpose of this article is to seek to provide guidance to tribunals by reviewing the available arbitral practice. This reveals that there are circumstances in which tribunals have adopted broadly consistent approaches to the status of the non-appearing witness's written testimony (although this does not appear to extend to the treatment of a non-appearing expert's evidence), and that tribunals have generally not distinguished between the existence of a valid reason for a witness's failure to appear, or of exceptional circumstances which would warrant the witness's evidence being admitted. In addition, tribunals appear to be reluctant to place much weight on a non-appearing witness's written evidence unless it is corroborated by the testimony of other witnesses or documentary evidence, and they are also reluctant to draw adverse inferences from a witness's non-appearance.
14 January 2020 in bioRxiv
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Preprint
Open access
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JHJessica A. Hall
Jessica A. Hall
DRDeepti Ramachandran
Deepti Ramachandran
HRHyun Cheol Roh
Hyun Cheol Roh
JDJoanna R. DiSpirito
Joanna R. DiSpirito
TBThiago Belchior
Thiago Belchior
ABAlex Banks
Alex Banks
Overnutrition and obesity promote adipose tissue dysfunction, often leading to systemic insulin resistance. The thiazolidinediones (TZDs) are a potent class of insulin-sensitizing drugs and ligands of PPARγ that improve insulin sensitivity, but their use is limited due to significant side effects. Recently, we demonstrated a mechanism by which TZDs improve insulin sensitivity distinct from receptor agonism and adipogenesis: reversal of obesity-linked phosphorylation of PPARγ at Serine 273. However, the role of this modification has not been tested genetically. Here we demonstrate that mice encoding an allele of PPARγ which cannot be phosphorylated at S273 are protected from insulin resistance, without exhibiting differences in body weight or TZD-associated side effects. Indeed, hyperinsulinemic-euglycemic clamp experiments confirm improved insulin sensitivity, as evidenced by increased whole-body glucose uptake. RNA-seq experiments reveal PPARγ S273 phosphorylation specifically enhances transcription of Gdf3, a BMP family member. Ectopic expression of Gdf3 is sufficient to induce insulin resistance in lean, healthy mice. We find that Gdf3 can impact metabolism by inhibition of BMP signaling. Together, these results highlight the diabetogenic role of PPARγ S273 phosphorylation and focuses attention on a putative target, Gdf3.
17 November 2011
Verified
Book Chapter
Closed access
CBChester W. Brown
Chester W. Brown
KMKate Miles
Kate Miles
Evolution in Investment Treaty Law and Arbitration - edited by Chester Brown November 2011