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Article ; Online: Reading Development in Children With Nonsyndromic Cleft Palate With or Without Cleft Lip: Meta-analysis and Systematic Review.

Lancaster, Hope Sparks / Lien, Kari M / Haas, Jordan / Ellis, Paige / Scherer, Nancy J

The Cleft palate-craniofacial journal : official publication of the American Cleft Palate-Craniofacial Association

2021 Volume 59, Issue 9, Page(s) 1155–1166

Abstract: Objective: We conducted a meta-analysis and systematic review of literature comparing pre-reading and general reading in school-age children with nonsyndromic cleft palate with or without cleft lip (NSCP/L) to their peers without NSCP/L.: Methods: ... ...

Abstract	Objective: We conducted a meta-analysis and systematic review of literature comparing pre-reading and general reading in school-age children with nonsyndromic cleft palate with or without cleft lip (NSCP/L) to their peers without NSCP/L. Methods: Our literature search identified 1238 possible records. After screening we identified 11 samples for inclusion for systematic review and eight for meta-analysis. We compared 292 children with NSCP/L to 311 peers for 23 pre-reading effect sizes and 17 general reading effect sizes (EF Results: On average school-age children with NSCP/L scored lower on pre-reading (EF Conclusions: Our findings suggest that school-age children with NSCP/L have persistent reading problems. Further research is needed to explore reading development in children with NSCP/L, as well as the relationships among hearing, speech, language, and reading development.
MeSH term(s)	Child ; Cleft Lip/epidemiology ; Cleft Palate/epidemiology ; Humans ; Reading
Language	English
Publishing date	2021-09-13
Publishing country	United States
Document type	Journal Article ; Meta-Analysis ; Systematic Review
ZDB-ID	1069409-2
ISSN	1545-1569 ; 0009-8701 ; 1055-6656
ISSN (online)	1545-1569
ISSN	0009-8701 ; 1055-6656
DOI	10.1177/10556656211039871
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Article ; Online: A microbial risk assessor's guide to Valley Fever (Coccidioides spp.): Case study and review of risk factors.

Kahn, David / Chen, William / Linden, Yarrow / Corbeil, Karalee A / Lowry, Sarah / Higham, Ciara A / Mendez, Karla S / Burch, Paige / DiFondi, Taylor / Verhougstraete, Marc / De Roos, Anneclaire J / Haas, Charles N / Gerba, Charles / Hamilton, Kerry A

The Science of the total environment

2024 Volume 917, Page(s) 170141

Abstract: Valley Fever is a respiratory disease caused by inhalation of arthroconidia, a type of spore produced by fungi within the genus Coccidioides spp. which are found in dry, hot ecosystems of the Western Hemisphere. A quantitative microbial risk assessment ( ... ...

Abstract	Valley Fever is a respiratory disease caused by inhalation of arthroconidia, a type of spore produced by fungi within the genus Coccidioides spp. which are found in dry, hot ecosystems of the Western Hemisphere. A quantitative microbial risk assessment (QMRA) for the disease has not yet been performed due to a lack of dose-response models and a scarcity of quantitative occurrence data from environmental samples. A literature review was performed to gather data on experimental animal dosing studies, environmental occurrence, human disease outbreaks, and meteorological associations. As a result, a risk framework is presented with information for parameterizing QMRA models for Coccidioides spp., with eight new dose-response models proposed. A probabilistic QMRA was conducted for a Southwestern US agricultural case study, evaluating eight scenarios related to farming occupational exposures. Median daily workday risks for developing severe Valley Fever ranged from 2.53 × 10
MeSH term(s)	Animals ; Humans ; Coccidioides ; Coccidioidomycosis/epidemiology ; Coccidioidomycosis/microbiology ; Ecosystem ; Risk Factors ; Risk Assessment
Language	English
Publishing date	2024-01-17
Publishing country	Netherlands
Document type	Review ; Journal Article
ZDB-ID	121506-1
ISSN	1879-1026 ; 0048-9697
ISSN (online)	1879-1026
ISSN	0048-9697
DOI	10.1016/j.scitotenv.2024.170141
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Article ; Online: The value of the patient perspective in understanding the full burden of migraine.

Wells, Rebecca Erwin / Estave, Paige M / Burch, Rebecca / Haas, Niina / Powers, Scott W / Seng, Elizabeth / Buse, Dawn C / Lipton, Richard B

Headache

2021 Volume 61, Issue 7, Page(s) 985–987

MeSH term(s)	Cost of Illness ; Guilt ; Humans ; Migraine Disorders/psychology ; Professional-Patient Relations ; Qualitative Research ; Social Stigma
Language	English
Publishing date	2021-08-07
Publishing country	United States
Document type	Editorial
ZDB-ID	410130-3
ISSN	1526-4610 ; 0017-8748
ISSN (online)	1526-4610
ISSN	0017-8748
DOI	10.1111/head.14167
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Article ; Online: Proteomic Approaches to Study SARS-CoV-2 Biology and COVID-19 Pathology.

Haas, Paige / Muralidharan, Monita / Krogan, Nevan J / Kaake, Robyn M / Hüttenhain, Ruth

Journal of proteome research

2021 Volume 20, Issue 2, Page(s) 1133–1152

Abstract: The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), was declared a pandemic infection in March 2020. As of December 2020, two COVID-19 vaccines have been authorized for ... ...

Abstract	The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), was declared a pandemic infection in March 2020. As of December 2020, two COVID-19 vaccines have been authorized for emergency use by the U.S. Food and Drug Administration, but there are no effective drugs to treat COVID-19, and pandemic mitigation efforts like physical distancing have had acute social and economic consequences. In this perspective, we discuss how the proteomic research community can leverage technologies and expertise to address the pandemic by investigating four key areas of study in SARS-CoV-2 biology. Specifically, we discuss how (1) mass spectrometry-based structural techniques can overcome limitations and complement traditional structural approaches to inform the dynamic structure of SARS-CoV-2 proteins, complexes, and virions; (2) virus-host protein-protein interaction mapping can identify the cellular machinery required for SARS-CoV-2 replication; (3) global protein abundance and post-translational modification profiling can characterize signaling pathways that are rewired during infection; and (4) proteomic technologies can aid in biomarker identification, diagnostics, and drug development in order to monitor COVID-19 pathology and investigate treatment strategies. Systems-level high-throughput capabilities of proteomic technologies can yield important insights into SARS-CoV-2 biology that are urgently needed during the pandemic, and more broadly, can inform coronavirus virology and host biology.
MeSH term(s)	COVID-19/epidemiology ; COVID-19/prevention & control ; COVID-19/virology ; Host-Pathogen Interactions ; Humans ; Mass Spectrometry/methods ; Pandemics ; Protein Interaction Maps ; Protein Processing, Post-Translational ; Proteome/metabolism ; Proteomics/methods ; SARS-CoV-2/metabolism ; SARS-CoV-2/physiology ; Viral Proteins/metabolism
Chemical Substances	Proteome ; Viral Proteins
Language	English
Publishing date	2021-01-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2078618-9
ISSN	1535-3907 ; 1535-3893
ISSN (online)	1535-3907
ISSN	1535-3893
DOI	10.1021/acs.jproteome.0c00764
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Article ; Online: CRISPR-Cas9 screen of E3 ubiquitin ligases identifies TRAF2 and UHRF1 as regulators of HIV latency in primary human T cells.

mBio

2024 Volume 15, Issue 4, Page(s) e0222223

Abstract: During HIV infection of CD4+ T cells, ubiquitin pathways are essential to viral replication and host innate immune response; however, the role of specific E3 ubiquitin ligases is not well understood. Proteomics analyses identified 116 single-subunit E3 ... ...

Abstract	During HIV infection of CD4+ T cells, ubiquitin pathways are essential to viral replication and host innate immune response; however, the role of specific E3 ubiquitin ligases is not well understood. Proteomics analyses identified 116 single-subunit E3 ubiquitin ligases expressed in activated primary human CD4+ T cells. Using a CRISPR-based arrayed spreading infectivity assay, we systematically knocked out 116 E3s from activated primary CD4+ T cells and infected them with NL4-3 GFP reporter HIV-1. We found 10 E3s significantly positively or negatively affected HIV infection in activated primary CD4+ T cells, including UHRF1 (pro-viral) and TRAF2 (anti-viral). Furthermore, deletion of either TRAF2 or UHRF1 in three JLat models of latency spontaneously increased HIV transcription. To verify this effect, we developed a CRISPR-compatible resting primary human CD4+ T cell model of latency. Using this system, we found that deletion of TRAF2 or UHRF1 initiated latency reactivation and increased virus production from primary human resting CD4+ T cells, suggesting these two E3s represent promising targets for future HIV latency reversal strategies. Importance: HIV, the virus that causes AIDS, heavily relies on the machinery of human cells to infect and replicate. Our study focuses on the host cell's ubiquitination system which is crucial for numerous cellular processes. Many pathogens, including HIV, exploit this system to enhance their own replication and survival. E3 proteins are part of the ubiquitination pathway that are useful drug targets for host-directed therapies. We interrogated the 116 E3s found in human immune cells known as CD4+ T cells, since these are the target cells infected by HIV. Using CRISPR, a gene-editing tool, we individually removed each of these enzymes and observed the impact on HIV infection in human CD4+ T cells isolated from healthy donors. We discovered that 10 of the E3 enzymes had a significant effect on HIV infection. Two of them, TRAF2 and UHRF1, modulated HIV activity within the cells and triggered an increased release of HIV from previously dormant or "latent" cells in a new primary T cell assay. This finding could guide strategies to perturb hidden HIV reservoirs, a major hurdle to curing HIV. Our study offers insights into HIV-host interactions, identifies new factors that influence HIV infection in immune cells, and introduces a novel methodology for studying HIV infection and latency in human immune cells.
MeSH term(s)	Humans ; CCAAT-Enhancer-Binding Proteins/metabolism ; CD4-Positive T-Lymphocytes ; CRISPR-Cas Systems ; HIV Infections ; TNF Receptor-Associated Factor 2/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitins/metabolism ; Virus Latency ; Virus Replication ; HIV/physiology
Chemical Substances	CCAAT-Enhancer-Binding Proteins ; TNF Receptor-Associated Factor 2 ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Ubiquitins ; UHRF1 protein, human (EC 2.3.2.27) ; PSMD2 protein, human
Language	English
Publishing date	2024-02-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mbio.02222-23
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Article ; Online: Mitochondrial dysfunction associated with TANGO2 deficiency.

Heiman, Paige / Mohsen, Al-Walid / Karunanidhi, Anuradha / St Croix, Claudette / Watkins, Simon / Koppes, Erik / Haas, Richard / Vockley, Jerry / Ghaloul-Gonzalez, Lina

Scientific reports

2022 Volume 12, Issue 1, Page(s) 3045

Abstract: Transport and Golgi Organization protein 2 Homolog (TANGO2)-related disease is an autosomal recessive disorder caused by mutations in the TANGO2 gene. Symptoms typically manifest in early childhood and include developmental delay, stress-induced episodic ...

Abstract	Transport and Golgi Organization protein 2 Homolog (TANGO2)-related disease is an autosomal recessive disorder caused by mutations in the TANGO2 gene. Symptoms typically manifest in early childhood and include developmental delay, stress-induced episodic rhabdomyolysis, and cardiac arrhythmias, along with severe metabolic crises including hypoglycemia, lactic acidosis, and hyperammonemia. Severity varies among and within families. Previous studies have reported contradictory evidence of mitochondrial dysfunction. Since the clinical symptoms and metabolic abnormalities are suggestive of a broad dysfunction of mitochondrial energy metabolism, we undertook a broad examination of mitochondrial bioenergetics in TANGO2 deficient patients utilizing skin fibroblasts derived from three patients exhibiting TANGO2-related disease. Functional studies revealed that TANGO2 protein was present in mitochondrial extracts of control cells but not patient cells. Superoxide production was increased in patient cells, while oxygen consumption rate, particularly under stress, along with relative ATP levels and β-oxidation of oleate were reduced. Our findings suggest that mitochondrial function should be assessed and monitored in all patients with TANGO2 mutation as targeted treatment of the energy dysfunction could improve outcome in this condition.
MeSH term(s)	Adolescent ; Adult ; Child ; Female ; Humans ; Male ; Aryl Hydrocarbon Receptor Nuclear Translocator/deficiency ; Aryl Hydrocarbon Receptor Nuclear Translocator/genetics ; Aryl Hydrocarbon Receptor Nuclear Translocator/metabolism ; Cells, Cultured ; Fatty Acids/metabolism ; Fibroblasts/metabolism ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondria/ultrastructure ; Mitochondrial Dynamics ; Mitochondrial Proteins/metabolism
Chemical Substances	ARNT protein, human ; Aryl Hydrocarbon Receptor Nuclear Translocator (138391-32-9) ; Fatty Acids ; Mitochondrial Proteins ; TANGO2 protein, human
Language	English
Publishing date	2022-02-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-07076-9
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Article ; Online: Mitochondrial dysfunction associated with TANGO2 deficiency

Paige Heiman / Al-Walid Mohsen / Anuradha Karunanidhi / Claudette St Croix / Simon Watkins / Erik Koppes / Richard Haas / Jerry Vockley / Lina Ghaloul-Gonzalez

Scientific Reports, Vol 12, Iss 1, Pp 1-

2022 Volume 11

Abstract: Abstract Transport and Golgi Organization protein 2 Homolog (TANGO2)-related disease is an autosomal recessive disorder caused by mutations in the TANGO2 gene. Symptoms typically manifest in early childhood and include developmental delay, stress-induced ...

Abstract	Abstract Transport and Golgi Organization protein 2 Homolog (TANGO2)-related disease is an autosomal recessive disorder caused by mutations in the TANGO2 gene. Symptoms typically manifest in early childhood and include developmental delay, stress-induced episodic rhabdomyolysis, and cardiac arrhythmias, along with severe metabolic crises including hypoglycemia, lactic acidosis, and hyperammonemia. Severity varies among and within families. Previous studies have reported contradictory evidence of mitochondrial dysfunction. Since the clinical symptoms and metabolic abnormalities are suggestive of a broad dysfunction of mitochondrial energy metabolism, we undertook a broad examination of mitochondrial bioenergetics in TANGO2 deficient patients utilizing skin fibroblasts derived from three patients exhibiting TANGO2-related disease. Functional studies revealed that TANGO2 protein was present in mitochondrial extracts of control cells but not patient cells. Superoxide production was increased in patient cells, while oxygen consumption rate, particularly under stress, along with relative ATP levels and β-oxidation of oleate were reduced. Our findings suggest that mitochondrial function should be assessed and monitored in all patients with TANGO2 mutation as targeted treatment of the energy dysfunction could improve outcome in this condition.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2022-02-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
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Article ; Online: A functional map of HIV-host interactions in primary human T cells.

Nature communications

2022 Volume 13, Issue 1, Page(s) 1752

Abstract: Human Immunodeficiency Virus (HIV) relies on host molecular machinery for replication. Systematic attempts to genetically or biochemically define these host factors have yielded hundreds of candidates, but few have been functionally validated in primary ... ...

Abstract	Human Immunodeficiency Virus (HIV) relies on host molecular machinery for replication. Systematic attempts to genetically or biochemically define these host factors have yielded hundreds of candidates, but few have been functionally validated in primary cells. Here, we target 426 genes previously implicated in the HIV lifecycle through protein interaction studies for CRISPR-Cas9-mediated knock-out in primary human CD4+ T cells in order to systematically assess their functional roles in HIV replication. We achieve efficient knockout (>50% of alleles) in 364 of the targeted genes and identify 86 candidate host factors that alter HIV infection. 47 of these factors validate by multiplex gene editing in independent donors, including 23 factors with restrictive activity. Both gene editing efficiencies and HIV-1 phenotypes are highly concordant among independent donors. Importantly, over half of these factors have not been previously described to play a functional role in HIV replication, providing numerous novel avenues for understanding HIV biology. These data further suggest that host-pathogen protein-protein interaction datasets offer an enriched source of candidates for functional host factor discovery and provide an improved understanding of the mechanics of HIV replication in primary T cells.
MeSH term(s)	CD4-Positive T-Lymphocytes/metabolism ; Gene Editing ; HIV Infections ; HIV-1/genetics ; Host Microbial Interactions/genetics ; Humans
Language	English
Publishing date	2022-04-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-29346-w
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Article ; Online: A functional map of HIV-host interactions in primary human T cells

Nature Communications, Vol 13, Iss 1, Pp 1-

2022 Volume 15

Abstract: Here, Hiatt et al. report the knock-out of over 400 genes in primary CD4+ T cells to assess their functional role in HIV replication, finding 86 initial candidates of which 47 are validated as HIV host factors, including 23 with restrictive activity. ...

Abstract	Here, Hiatt et al. report the knock-out of over 400 genes in primary CD4+ T cells to assess their functional role in HIV replication, finding 86 initial candidates of which 47 are validated as HIV host factors, including 23 with restrictive activity.
Keywords	Science ; Q
Language	English
Publishing date	2022-04-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
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Article ; Online: Chemogenetic Characterization of Inositol Phosphate Metabolic Pathway Reveals Druggable Enzymes for Targeting Kinetoplastid Parasites.

Cestari, Igor / Haas, Paige / Moretti, Nilmar Silvio / Schenkman, Sergio / Stuart, Ken

Cell chemical biology

2016 Volume 23, Issue 5, Page(s) 608–617

Abstract: Kinetoplastids cause Chagas disease, human African trypanosomiasis, and leishmaniases. Current treatments for these diseases are toxic and inefficient, and our limited knowledge of drug targets and inhibitors has dramatically hindered the development of ... ...

Abstract	Kinetoplastids cause Chagas disease, human African trypanosomiasis, and leishmaniases. Current treatments for these diseases are toxic and inefficient, and our limited knowledge of drug targets and inhibitors has dramatically hindered the development of new drugs. Here we used a chemogenetic approach to identify new kinetoplastid drug targets and inhibitors. We conditionally knocked down Trypanosoma brucei inositol phosphate (IP) pathway genes and showed that almost every pathway step is essential for parasite growth and infection. Using a genetic and chemical screen, we identified inhibitors that target IP pathway enzymes and are selective against T. brucei. Two series of these inhibitors acted on T. brucei inositol polyphosphate multikinase (IPMK) preventing Ins(1,4,5)P3 and Ins(1,3,4,5)P4 phosphorylation. We show that IPMK is functionally conserved among kinetoplastids and that its inhibition is also lethal for Trypanosoma cruzi. Hence, IP enzymes are viable drug targets in kinetoplastids, and IPMK inhibitors may aid the development of new drugs.
MeSH term(s)	Animals ; Dose-Response Relationship, Drug ; HeLa Cells ; Hep G2 Cells ; Humans ; Inositol Phosphates/antagonists & inhibitors ; Inositol Phosphates/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Parasites/drug effects ; Parasites/enzymology ; Phosphotransferases (Alcohol Group Acceptor)/antagonists & inhibitors ; Phosphotransferases (Alcohol Group Acceptor)/genetics ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; Protein Kinase Inhibitors/chemistry ; Protein Kinase Inhibitors/pharmacology ; Structure-Activity Relationship ; Trypanosoma brucei brucei/drug effects ; Trypanosoma brucei brucei/enzymology ; Trypanosoma brucei brucei/growth & development ; Tumor Cells, Cultured
Chemical Substances	Inositol Phosphates ; Protein Kinase Inhibitors ; Phosphotransferases (Alcohol Group Acceptor) (EC 2.7.1.-) ; inositol polyphosphate multikinase (EC 2.7.1.-)
Language	English
Publishing date	2016--19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ISSN	2451-9448
ISSN (online)	2451-9448
DOI	10.1016/j.chembiol.2016.03.015
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