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Article ; Online: Infections diagnosed in children and young people screened for malaria in UK emergency departments: a retrospective multi-centre study.

Bird, Chris / Hayward, Gail N / Turner, Philip J / Wasala, Desha / Merrick, Vanessa / Lyttle, Mark D / Mullen, Niall / Fanshawe, Thomas R

Paediatrics and international child health

2024 Volume 44, Issue 1, Page(s) 1–7

Abstract: Background: Data on imported infections in children and young people (CYP) are sparse.: Aims: To describe imported infections in CYP arriving from malaria-endemic areas and presenting to UK emergency departments (ED) who were screened for malaria.: ...

Abstract	Background: Data on imported infections in children and young people (CYP) are sparse. Aims: To describe imported infections in CYP arriving from malaria-endemic areas and presenting to UK emergency departments (ED) who were screened for malaria. Methods: This is a retrospective, multi-centre, observational study nested in a diagnostic accuracy study for malaria rapid diagnostic tests. Any CYP < 16 years presenting to a participating ED with a history of fever and travel to a malaria-endemic area between 1 January 2016 and 31 December 2017 and who had a malaria screen as a part of standard care were included. Geographical risk was calculated for the most common tropical infections. Results: Of the 1414 CYP screened for malaria, 44.0% ( Conclusion: A fifth of CYP presenting to participating UK EDs with fever and a history of travel to a malaria-endemic area and who were screened for malaria had a tropical infection if diarrhoea is included. A third of CYP had no diagnosis. CYP arriving from sub-Saharan Africa had the greatest risk of malaria.
MeSH term(s)	Child ; Humans ; Adolescent ; Retrospective Studies ; Communicable Diseases, Imported/diagnosis ; Communicable Diseases, Imported/epidemiology ; Malaria/diagnosis ; Malaria/epidemiology ; Fever ; Emergency Service, Hospital ; United Kingdom/epidemiology
Language	English
Publishing date	2024-01-11
Publishing country	England
Document type	Observational Study ; Multicenter Study ; Journal Article
ZDB-ID	2649065-1
ISSN	2046-9055 ; 2046-9047
ISSN (online)	2046-9055
ISSN	2046-9047
DOI	10.1080/20469047.2023.2299576
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Article ; Online: TREM2 variants that cause early dementia and increase Alzheimer's disease risk affect gene splicing.

Kiianitsa, Kostantin / Lukes, Maria E / Hayes, Brian J / Brutman, Julianna / Valdmanis, Paul N / Bird, Thomas D / Raskind, Wendy H / Korvatska, Olena

Brain : a journal of neurology

2024

Abstract: Loss-of-function variants in the triggering receptor expressed on myeloid cells 2 (TREM2) are responsible for a spectrum of neurodegenerative disorders. In the homozygous state, they cause severe pathologies with early onset dementia, such as Nasu-Hakola ...

Abstract	Loss-of-function variants in the triggering receptor expressed on myeloid cells 2 (TREM2) are responsible for a spectrum of neurodegenerative disorders. In the homozygous state, they cause severe pathologies with early onset dementia, such as Nasu-Hakola disease (NHD) and behavioral variants of frontotemporal dementia (FTD), whereas heterozygous variants increase the risk of late-onset Alzheimer's disease (AD) and FTD. For over half of TREM2 variants found in families with recessive early onset dementia, the defect occurs at the transcript level via premature termination codons or aberrant splicing. The remaining variants are missense alterations thought to affect the protein; however, the underlying pathogenic mechanism is less clear. In this work, we tested whether these disease-associated TREM2 variants contribute to the pathology via altered splicing. Variants scored by SpliceAI algorithm were tested by a full-size TREM2 splicing reporter assay in different cell lines. The effect of variants was quantified by qRT-/RT-PCR and western blots. Nanostring nCounter was used to measure TREM2 RNA in the brains of NHD patients who carried spliceogenic variants. Exon skipping events were analyzed from brain RNA-Seq datasets available through the Accelerating Medicines Partnership for Alzheimer's Disease Consortium (AMP-AD). We found that for some NHD and early onset FTD-causing variants, splicing defects were the primary cause (D134G) or likely contributor to pathogenicity (V126G and K186N). Similar but milder effects on splicing of exons 2 and 3 were demonstrated for A130V, L133L and R136W enriched in patients with dementia. Moreover, the two most frequent missense variants associated with AD/FTD risk in European and African ancestries (R62H, 1% in Caucasians, and T96K, 12% in Africans) had splicing defects via excessive skipping of exon 2 and overproduction of a potentially antagonistic TREM2 protein isoform. The effect of R62H on exon 2 skipping was confirmed in three independent brain RNA-seq datasets. Our findings revealed an unanticipated complexity of pathogenic variation in TREM2, in which effects on post-transcriptional gene regulation and protein function often coexist. This necessitates the inclusion of computational and experimental analyses of splicing and mRNA processing for a better understanding of genetic variation in disease.
Language	English
Publishing date	2024-01-16
Publishing country	England
Document type	Journal Article
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awae014
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Article: Clinical approach to the patient with neurogenetic disease.

Bird, Thomas D / Smith, Corrie O

Handbook of clinical neurology

2018 Volume 147, Page(s) 3–9

Abstract: Neurogenetic diseases are surprisingly common. This chapter reviews a systematic approach to the evaluation of a patient thought to have such a disease. The emphasis is on first recognizing potential clues to the diagnosis contained in the family history ...

Abstract	Neurogenetic diseases are surprisingly common. This chapter reviews a systematic approach to the evaluation of a patient thought to have such a disease. The emphasis is on first recognizing potential clues to the diagnosis contained in the family history and presentation of symptoms. Ataxia, neuropathy, muscle weakness, dementia, epilepsy, and cognitive delay are all "reservoirs" of neurogenetic disease. A high index of suspicion for genetic causes and a thoughtful evaluation of simplex (sporadic) cases is often necessary. Then the physician can proceed to the differential diagnosis, genetic testing, and genetic counseling. A team approach including a genetic counselor is usually the best strategy.
MeSH term(s)	Family Health ; Genetic Counseling ; Genetic Predisposition to Disease/genetics ; Genetic Testing/methods ; Humans ; Nervous System Diseases/diagnosis ; Nervous System Diseases/genetics ; Nervous System Diseases/therapy
Language	English
Publishing date	2018
Publishing country	Netherlands
Document type	Journal Article ; Review
ISSN	0072-9752
ISSN	0072-9752
DOI	10.1016/B978-0-444-63233-3.00001-4
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Article: Progress in Amyotrophic Lateral Sclerosis Gene Discovery: Reflecting on Classic Approaches and Leveraging Emerging Technologies.

Smukowski, Samuel N / Maioli, Heather / Latimer, Caitlin S / Bird, Thomas D / Jayadev, Suman / Valdmanis, Paul N

Neurology. Genetics

2022 Volume 8, Issue 3, Page(s) e669

Abstract: Amyotrophic lateral sclerosis (ALS) is the most prominent motor neuron disease in humans. Its etiology consists of progressive motor neuron degeneration resulting in a rapid decline in motor function starting in the limbs or bulbar muscles and eventually ...

Abstract	Amyotrophic lateral sclerosis (ALS) is the most prominent motor neuron disease in humans. Its etiology consists of progressive motor neuron degeneration resulting in a rapid decline in motor function starting in the limbs or bulbar muscles and eventually fatally impairing central organs most typically resulting in loss of respiration. Pathogenic variants in 4 main genes,
Language	English
Publishing date	2022-04-27
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2818607-2
ISSN	2376-7839
ISSN	2376-7839
DOI	10.1212/NXG.0000000000000669
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Article ; Online: TREM2 and neurodegenerative disease.

Bird, Thomas D

The New England journal of medicine

2013 Volume 369, Issue 16, Page(s) 1568

MeSH term(s)	Alzheimer Disease/genetics ; Animals ; Humans ; Membrane Glycoproteins/genetics ; Mutation ; Mutation, Missense ; Receptors, Immunologic/genetics
Chemical Substances	Membrane Glycoproteins ; Receptors, Immunologic
Language	English
Publishing date	2013-10-17
Publishing country	United States
Document type	Comment ; Letter
ZDB-ID	207154-x
ISSN	1533-4406 ; 0028-4793
ISSN (online)	1533-4406
ISSN	0028-4793
DOI	10.1056/NEJMc1306509#SA5
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Article ; Online: Aberrant splicing of PSEN2, but not PSEN1, in individuals with sporadic Alzheimer's disease.

Course, Meredith M / Gudsnuk, Kathryn / Keene, C Dirk / Bird, Thomas D / Jayadev, Suman / Valdmanis, Paul N

Brain : a journal of neurology

2022 Volume 146, Issue 2, Page(s) 507–518

Abstract: Alzheimer's disease is the most common neurodegenerative disease, characterized by dementia and premature death. Early-onset familial Alzheimer's disease is caused in part by pathogenic variants in presenilin 1 (PSEN1) and presenilin 2 (PSEN2), and ... ...

Abstract	Alzheimer's disease is the most common neurodegenerative disease, characterized by dementia and premature death. Early-onset familial Alzheimer's disease is caused in part by pathogenic variants in presenilin 1 (PSEN1) and presenilin 2 (PSEN2), and alternative splicing of these two genes has been implicated in both familial and sporadic Alzheimer's disease. Here, we leveraged targeted isoform-sequencing to characterize thousands of complete PSEN1 and PSEN2 transcripts in the prefrontal cortex of individuals with sporadic Alzheimer's disease, familial Alzheimer's disease (carrying PSEN1 and PSEN2 variants), and controls. Our results reveal alternative splicing patterns of PSEN2 specific to sporadic Alzheimer's disease, including a human-specific cryptic exon present in intron 9 of PSEN2 as well as a 77 bp intron retention product before exon 6 that are both significantly elevated in sporadic Alzheimer's disease samples, alongside a significantly lower percentage of canonical full-length PSEN2 transcripts versus familial Alzheimer's disease samples and controls. Both alternatively spliced products are predicted to generate a prematurely truncated PSEN2 protein and were corroborated in an independent cerebellum RNA-sequencing dataset. In addition, our data in PSEN variant carriers is consistent with the hypothesis that PSEN1 and PSEN2 variants need to produce full-length but variant proteins to contribute to the onset of Alzheimer's disease, although intriguingly there were far fewer full-length transcripts carrying pathogenic alleles versus wild-type alleles in PSEN2 variant carriers. Finally, we identify frequent RNA editing at Alu elements present in an extended 3' untranslated region in PSEN2. Overall, this work expands the understanding of PSEN1 and PSEN2 variants in Alzheimer's disease, shows that transcript differences in PSEN2 may play a role in sporadic Alzheimer's disease, and suggests novel mechanisms of Alzheimer's disease pathogenesis.
MeSH term(s)	Humans ; Alzheimer Disease/genetics ; Amyloid beta-Protein Precursor/genetics ; Mutation ; Presenilin-2/genetics ; Presenilin-1/genetics ; Neurodegenerative Diseases
Chemical Substances	Amyloid beta-Protein Precursor ; Presenilin-2 ; Presenilin-1 ; PSEN2 protein, human
Language	English
Publishing date	2022-08-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awac294
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Article ; Online: Impacts of metal mining on river systems: a global assessment.

Macklin, M G / Thomas, C J / Mudbhatkal, A / Brewer, P A / Hudson-Edwards, K A / Lewin, J / Scussolini, P / Eilander, D / Lechner, A / Owen, J / Bird, G / Kemp, D / Mangalaa, K R

Science (New York, N.Y.)

2023 Volume 381, Issue 6664, Page(s) 1345–1350

Abstract: An estimated 23 million people live on floodplains affected by potentially dangerous concentrations of toxic waste derived from past and present metal mining activity. We analyzed the global dimensions of this hazard, particularly in regard to lead, zinc, ...

Abstract	An estimated 23 million people live on floodplains affected by potentially dangerous concentrations of toxic waste derived from past and present metal mining activity. We analyzed the global dimensions of this hazard, particularly in regard to lead, zinc, copper, and arsenic, using a georeferenced global database detailing all known metal mining sites and intact and failed tailings storage facilities. We then used process-based and empirically tested modeling to produce a global assessment of metal mining contamination in river systems and the numbers of human populations and livestock exposed. Worldwide, metal mines affect 479,200 kilometers of river channels and 164,000 square kilometers of floodplains. The number of people exposed to contamination sourced from long-term discharge of mining waste into rivers is almost 50 times greater than the number directly affected by tailings dam failures.
Language	English
Publishing date	2023-09-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.adg6704
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Article ; Online: A Diagnostic Accuracy Study to Evaluate Standard Rapid Diagnostic Test (RDT) Alone to Safely Rule Out Imported Malaria in Children Presenting to UK Emergency Departments.

Bird, Chris / Hayward, Gail N / Turner, Philip J / Merrick, Vanessa / Lyttle, Mark D / Mullen, Niall / Fanshawe, Thomas R

Journal of the Pediatric Infectious Diseases Society

2023 Volume 12, Issue 5, Page(s) 290–297

Abstract: Background: Microscopy is the gold standard for malaria diagnosis but is dependent on trained personnel. Rapid diagnostic tests (RDTs) form the mainstay of diagnosis in endemic areas without access to high-quality microscopy. We aimed to evaluate ... ...

Abstract	Background: Microscopy is the gold standard for malaria diagnosis but is dependent on trained personnel. Rapid diagnostic tests (RDTs) form the mainstay of diagnosis in endemic areas without access to high-quality microscopy. We aimed to evaluate whether RDT alone could rule out imported malaria in children presenting to UK emergency departments (EDs). Methods: UK-based, multi-center, retrospective, diagnostic accuracy study. Included: any child <16 years presenting to ED with history of fever and travel to a malaria-endemic country, between 01/01/2016 and 31/12/2017. Diagnosis: microscopy for malarial parasites (clinical reference standard) and RDT (index test). UK Health Research Authority approval: 20/HRA/1341. Results: There were 47 cases of malaria out of 1,414 eligible cases (prevalence 3.3%) in a cohort of children whose median age was 4 years (IQR 2-9), of whom 43% were female. Cases of Plasmodium falciparum totaled 36 (77%, prevalence 2.5%). The sensitivity of RDT alone to detect malaria infection due to any Plasmodium species was 93.6% (95% CI 82.5-98.7%), specificity 99.4% (95% CI 98.9-99.7%), positive predictive value 84.6% (95% CI 71.9-93.1%) and negative predictive value 99.8% (95% CI 99.4-100.0%). Sensitivity of RDT to detect P. falciparum infection was 100% (90.3-100%), specificity 98.8% (98.1-99.3%), positive predictive value 69.2% (54.9-81.2%, n = 46/52) and negative predictive value 100% (99.7-100%, n = 1,362/1,362). Conclusions: RDTs were 100% sensitive in detecting P. falciparum malaria. However, lower sensitivity for other malaria species and the rise of pfhrp2 and pfhrp3 (pfhrp2/3) gene deletions in the P. falciparum parasite mandate the continued use of microscopy for diagnosing malaria.
MeSH term(s)	Child ; Humans ; Female ; Child, Preschool ; Male ; Antigens, Protozoan ; Protozoan Proteins ; Rapid Diagnostic Tests ; Retrospective Studies ; Polymerase Chain Reaction ; Malaria/diagnosis ; Malaria, Falciparum/diagnosis ; Malaria, Falciparum/epidemiology ; United Kingdom ; Diagnostic Tests, Routine ; Sensitivity and Specificity
Chemical Substances	Antigens, Protozoan ; Protozoan Proteins
Language	English
Publishing date	2023-04-18
Publishing country	England
Document type	Journal Article
ZDB-ID	2668791-4
ISSN	2048-7207 ; 2048-7193
ISSN (online)	2048-7207
ISSN	2048-7193
DOI	10.1093/jpids/piad024
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Article ; Online: Survival of the Aequalis total shoulder replacement at a minimum 20-year follow-up: a clinical and radiographic study.

Evans, Jonathan P / Batten, Timothy / Bird, Joshua / Thomas, William J / Kitson, Jeff B / Smith, Christopher D

Journal of shoulder and elbow surgery

2021 Volume 30, Issue 10, Page(s) 2355–2360

Abstract: Aims: Shoulder replacement is increasingly performed for end-stage arthritis. Information on the long-term survival and patient outcomes is very limited. This study aimed to quantify the survival and clinical outcome at a minimum of 20-yr follow-up.: ... ...

Abstract	Aims: Shoulder replacement is increasingly performed for end-stage arthritis. Information on the long-term survival and patient outcomes is very limited. This study aimed to quantify the survival and clinical outcome at a minimum of 20-yr follow-up. Methods: A single-center, single-surgeon, consecutive cohort study was performed. Forty-four shoulder replacements in 40 patients (age at surgery 68.5 years, 82.5% female, preoperative visual analog scale [VAS] pain score 5.1/10, standard deviation [SD] 2.7) implanted between 1996 and 2000 were assessed. All-cause construct survival, radiographic glenoid and humeral stem loosening, radiographic humeral head migration, and patient-reported outcome measures were assessed. Results: Survival with all-cause revision as an endpoint was 84.1% (95% confidence interval [CI] 60.7, 94.1) at 20 years, glenoid loosening was seen in all patients who survived to the 20-year follow-up. Survival of rotator cuff integrity was 16.8% (95% CI 3.5, 38.5) at 20 years. VAS pain scores demonstrated improvement at 10 years (mean change -4/10) but not at 20 years (effect size -0.15, mean change 0.4/10, SD 2.7). At 20 years, 72% of patients had died with the prosthesis in situ. Conclusion: Older patients undergoing total shoulder arthroplasty are unlikely to require revision in their lifetime. However, beyond 10 years, a large proportion of implants demonstrate glenoid loosening, humeral head migration, and declining patient outcomes. This information will be of use to patients and clinicians when discussing the potential outcomes of surgery.
Language	English
Publishing date	2021-03-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	1170782-3
ISSN	1532-6500 ; 1058-2746
ISSN (online)	1532-6500
ISSN	1058-2746
DOI	10.1016/j.jse.2021.01.038
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Article ; Online: A familial missense variant in the Alzheimer's disease gene SORL1 impairs its maturation and endosomal sorting.

Fazeli, Elnaz / Child, Daniel D / Bucks, Stephanie A / Stovarsky, Miki / Edwards, Gabrielle / Rose, Shannon E / Yu, Chang-En / Latimer, Caitlin / Kitago, Yu / Bird, Thomas / Jayadev, Suman / Andersen, Olav M / Young, Jessica E

Acta neuropathologica

2024 Volume 147, Issue 1, Page(s) 20

Abstract: The SORL1 gene has recently emerged as a strong Alzheimer's Disease (AD) risk gene. Over 500 different variants have been identified in the gene and the contribution of individual variants to AD development and progression is still largely unknown. Here, ...

Abstract	The SORL1 gene has recently emerged as a strong Alzheimer's Disease (AD) risk gene. Over 500 different variants have been identified in the gene and the contribution of individual variants to AD development and progression is still largely unknown. Here, we describe a family consisting of 2 parents and 5 offspring. Both parents were affected with dementia and one had confirmed AD pathology with an age of onset > 75 years. All offspring were affected with AD with ages at onset ranging from 53 years to 74 years. DNA was available from the parent with confirmed AD and 5 offspring. We identified a coding variant, p.(Arg953Cys), in SORL1 in 5 of 6 individuals affected by AD. Notably, variant carriers had severe AD pathology, and the SORL1 variant segregated with TDP-43 pathology (LATE-NC). We further characterized this variant and show that this Arginine substitution occurs at a critical position in the YWTD-domain of the SORL1 translation product, SORL1. Functional studies further show that the p.R953C variant leads to retention of the SORL1 protein in the endoplasmic reticulum which leads to decreased maturation and shedding of the receptor and prevents its normal endosomal trafficking. Together, our analysis suggests that p.R953C is a pathogenic variant of SORL1 and sheds light on mechanisms of how missense SORL1 variants may lead to AD.
MeSH term(s)	Humans ; Aged ; Alzheimer Disease/genetics ; Gene Frequency ; Genetic Predisposition to Disease ; Membrane Transport Proteins/genetics ; Mutation, Missense ; LDL-Receptor Related Proteins/genetics ; Polymorphism, Single Nucleotide
Chemical Substances	Membrane Transport Proteins ; LDL-Receptor Related Proteins ; SORL1 protein, human
Language	English
Publishing date	2024-01-20
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1079-0
ISSN	1432-0533 ; 0001-6322
ISSN (online)	1432-0533
ISSN	0001-6322
DOI	10.1007/s00401-023-02670-1
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