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Article ; Online: Dual diagnosis of autosomal dominant polycystic kidney disease and sickle cell disease in a teenage male.

Stein, Quinn / Herman, Kathleen / Deyo, Jennifer / McDonough, Colleen / Bloom, Michelle S / Mansuri, Asifhusen

2023 Volume 38, Issue 9, Page(s) 3189–3192

Abstract: Background: Sickle cell disease (SCD) and autosomal dominant polycystic kidney disease (ADPKD) are relatively common genetic conditions with considerable overlap in clinical presentation. In addition to similarities between the signs and symptoms in ... ...

Abstract	Background: Sickle cell disease (SCD) and autosomal dominant polycystic kidney disease (ADPKD) are relatively common genetic conditions with considerable overlap in clinical presentation. In addition to similarities between the signs and symptoms in sickle cell nephropathy and ADPKD, more than half of SCD patients have kidney cysts. The co-occurrence of these two diseases has not been previously reported in the literature. Case diagnosis/treatment: A 16-year-old Black male with SCD had bilateral kidney enlargement and multiple simple cysts on ultrasound. Although kidney cysts are significantly more common in individuals affected with SCD, genetic testing with a broad kidney gene panel was performed to explore the possible presence of another underlying genetic cause of his cysts, in addition to SCD. A dual diagnosis of SCD and ADPKD was made following the identification of two copies of the common pathogenic sickle cell HBB variant (c.20A > T, p.Glu7Val) and a pathogenic missense variant in PKD1 (c.8311G > A, p.Glu2771Lys). Conclusions: SCD and ADPKD differ in pathophysiological mechanisms and treatment regimens. As such, it will be paramount for this teenager to be closely monitored for signs of diminished kidney function and to be co-managed as he transitions to adult care to ensure proper treatment and management. Early identification of individuals with both SCD and a co-occurring condition is crucial to ensuring proper clinical management. Furthermore, identifying and reporting additional patients with SCD and ADPKD dual diagnoses will help us to understand the co-occurring disease course and optimal treatments.
MeSH term(s)	Adult ; Humans ; Male ; Adolescent ; Polycystic Kidney, Autosomal Dominant/complications ; Polycystic Kidney, Autosomal Dominant/diagnosis ; Polycystic Kidney, Autosomal Dominant/genetics ; Diagnosis, Dual (Psychiatry) ; Kidney Neoplasms ; Anemia, Sickle Cell/complications ; Anemia, Sickle Cell/diagnosis ; Anemia, Sickle Cell/genetics ; Cysts ; TRPP Cation Channels/genetics
Chemical Substances	TRPP Cation Channels
Language	English
Publishing date	2023-01-16
Publishing country	Germany
Document type	Journal Article
ZDB-ID	631932-4
ISSN	1432-198X ; 0931-041X
ISSN (online)	1432-198X
ISSN	0931-041X
DOI	10.1007/s00467-023-05873-6
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Article: A Specialized Centrosome-Proteasome Axis Mediates Proteostasis and Influences Cardiac Stress through Txlnb.

McLendon, Jared M / Zhang, Xiaoming / Stein, Colleen S / Baehr, Leslie M / Bodine, Sue C / Boudreau, Ryan L

bioRxiv : the preprint server for biology

2024

Abstract: Background: Centrosomes localize to perinuclear foci where they serve multifunctional roles, arranging the microtubule organizing center (MTOC) and anchoring ubiquitin-proteasome system (UPS) machinery. In mature cardiomyocytes, centrosomal proteins ... ...

Abstract	Background: Centrosomes localize to perinuclear foci where they serve multifunctional roles, arranging the microtubule organizing center (MTOC) and anchoring ubiquitin-proteasome system (UPS) machinery. In mature cardiomyocytes, centrosomal proteins redistribute into a specialized perinuclear cage-like structure, and a potential centrosome-UPS interface has not been studied. Taxilin-beta (Txlnb), a cardiomyocyte-enriched protein, belongs to a family of centrosome adapter proteins implicated in protein quality control. We hypothesize that Txlnb plays a key role in centrosomal-proteasomal crosstalk in cardiomyocytes. Methods: Integrative bioinformatics assessed centrosomal gene dysregulation in failing hearts. Txlnb gain/loss-of-function studies were conducted in cultured cardiomyocytes and mice. Txlnb's role in cardiac proteotoxicity and hypertrophy was examined using CryAB-R120G mice and transverse aortic constriction (TAC), respectively. Molecular modeling investigated Txlnb structure/function. Results: Human failing hearts show consistent dysregulation of many centrosome-associated genes, alongside UPS-related genes. Txlnb emerged as a candidate regulator of cardiomyocyte proteostasis that localizes to the perinuclear centrosomal compartment. Txlnb's interactome strongly supports its involvement in cytoskeletal, microtubule, and UPS processes, particularly centrosome-related functions. Overexpressing Txlnb in cardiomyocytes reduced ubiquitinated protein accumulation and enhanced proteasome activity during hypertrophy. Txlnb-knockout (KO) mouse hearts exhibit proteasomal insufficiency and altered cardiac growth, evidenced by ubiquitinated protein accumulation, decreased 26Sβ5 proteasome activity, and lower mass with age. In Cryab-R120G mice, Txlnb loss worsened heart failure, causing lower ejection fractions. After TAC, Txlnb-KO mice also showed reduced ejection fraction, increased heart mass, and elevated ubiquitinated protein accumulation. Investigations into the molecular mechanisms revealed that Txlnb-KO did not affect proteasomal subunit expression but led to the upregulation of Txlna and several centrosomal proteins (Cep63, Ofd1, and Tubg) suggesting altered centrosomal dynamics. Structural predictions support Txlnb's role as a specialized centrosomal-adapter protein bridging centrosomes with proteasomes, confirmed by microtubule-dependent perinuclear localization. Conclusions: Together, these data provide initial evidence connecting Txlnb to cardiac proteostasis, hinting at the potential importance of functional bridging between specialized centrosomes and UPS in cardiomyocytes.
Language	English
Publishing date	2024-02-14
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.02.12.580020
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Article ; Online: Implementation Strategy Fidelity and Organizational Outcomes in a Randomized Trial: Implications for Reentry from Corrections to Community Treatment.

Stein, L A R / Bassett, Shayna S / Welsh, Wayne N / Clair-Michaud, Mary / Abdel-Salam, Sami / Monico, Laura / Gallagher, Colleen / Murgo, Cecilia / Yang, Yang / Friedmann, Peter D / Clarke, Jennifer G

Substance use & misuse

2023 Volume 58, Issue 3, Page(s) 320–330

Abstract: Background: ...

Abstract	Background:
MeSH term(s)	Humans ; Evidence-Based Practice ; Prisoners ; Substance-Related Disorders ; Leadership
Language	English
Publishing date	2023-01-11
Publishing country	England
Document type	Randomized Controlled Trial ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S. ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1310358-1
ISSN	1532-2491 ; 1082-6084
ISSN (online)	1532-2491
ISSN	1082-6084
DOI	10.1080/10826084.2022.2161311
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Article: Modulation of miR-181 influences dopaminergic neuronal degeneration in a mouse model of Parkinson's disease.

Stein, Colleen S / McLendon, Jared M / Witmer, Nathan H / Boudreau, Ryan L

Molecular therapy. Nucleic acids

2022 Volume 28, Page(s) 1–15

Abstract: Parkinson's disease (PD) is caused by the loss of dopaminergic (DA) neurons in the substantia nigra (SN). Although PD pathogenesis is not fully understood, studies implicate perturbations in gene regulation, mitochondrial function, and neuronal activity. ...

Abstract	Parkinson's disease (PD) is caused by the loss of dopaminergic (DA) neurons in the substantia nigra (SN). Although PD pathogenesis is not fully understood, studies implicate perturbations in gene regulation, mitochondrial function, and neuronal activity. MicroRNAs (miRs) are small gene regulatory RNAs that inhibit diverse subsets of target mRNAs, and several studies have noted miR expression alterations in PD brains. For example, miR-181a is abundant in the brain and is increased in PD patient brain samples; however, the disease relevance of this remains unclear. Here, we show that miR-181 target mRNAs are broadly downregulated in aging and PD brains. To address whether the miR-181 family plays a role in PD pathogenesis, we generated adeno-associated viruses (AAVs) to overexpress and inhibit the miR-181 isoforms. After co-injection with AAV overexpressing alpha-synuclein (aSyn) into mouse SN (PD model), we found that moderate miR-181a/b overexpression exacerbated aSyn-induced DA neuronal loss, whereas miR-181 inhibition was neuroprotective relative to controls (GFP alone and/or scrambled RNA). Also, prolonged miR-181 overexpression in SN alone elicited measurable neurotoxicity that is coincident with an increased immune response. mRNA-seq analyses revealed that miR-181a/b inhibits genes involved in synaptic transmission, neurite outgrowth, and mitochondrial respiration, along with several genes having known protective roles and genetic links in PD.
Language	English
Publishing date	2022-02-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	2662631-7
ISSN	2162-2531
ISSN	2162-2531
DOI	10.1016/j.omtn.2022.02.007
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Article ; Online: A survey of the assistive technology experience of older adults in Tompkins County, NY.

Vitlin-Stein, Isabella / Gitlow, Lynn / Fusco, Brianna / Pathammavong, Sabrina / Rajotte, Colleen

Disability and rehabilitation. Assistive technology

2024 , Page(s) 1–7

Abstract: Purpose: ...

Abstract	Purpose:
Language	English
Publishing date	2024-03-19
Publishing country	England
Document type	Journal Article
ZDB-ID	2221782-4
ISSN	1748-3115 ; 1748-3107
ISSN (online)	1748-3115
ISSN	1748-3107
DOI	10.1080/17483107.2024.2330086
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Article: Female-specific risk factors of parity and menopause age and risk of carotid plaque: the multi-ethnic study of atherosclerosis.

Rodriguez, Carla P / Ogunmoroti, Oluseye / Minhas, Anum S / Vaidya, Dhananjay / Kazzi, Brigitte / Osibogun, Olatokunbo / Whelton, Seamus / Kovell, Lara C / Harrington, Colleen M / Honigberg, Michael C / Thamman, Ritu / Stein, James H / Shapiro, Michael D / Michos, Erin D

American journal of cardiovascular disease

2023 Volume 13, Issue 4, Page(s) 222–234

Abstract: Background: Female-specific factors of grand multiparity (≥5 births) and early menopause age are associated with an increased risk of cardiovascular disease (CVD). However, mechanisms are incompletely understood. Carotid plaque is a marker of ... ...

Abstract	Background: Female-specific factors of grand multiparity (≥5 births) and early menopause age are associated with an increased risk of cardiovascular disease (CVD). However, mechanisms are incompletely understood. Carotid plaque is a marker of subclinical atherosclerosis and associated with increased CVD risk. We evaluated the association of female-specific factors with plaque burden. Methods: We included 2,313 postmenopausal women in the Multi-Ethnic Study of Atherosclerosis, free of clinical CVD, whose parity and menopause age were ascertained by questionnaires and carotid plaque measured by ultrasound at baseline and 10 years later. Parity was categorized as nulliparity (reference), 1-2, 3-4 and ≥5 live births. Menopause age was categorized as <45, 45-49, 50-54 (reference) and ≥55 years. Multivariable regression was performed to evaluate the association of parity and menopause age with carotid plaque presence (yes/no) and extent [carotid plaque score (CPS)]. Results: The mean age was 64±9 years; 52.3% had prevalent carotid plaque at baseline. Compared to nulliparity, grand multiparity was significantly associated with prevalent carotid plaque after adjustment for CVD risk factors (prevalence ratio 1.17 (95% CI 1.03-1.35)) and progression of CPS over 10 years [percent difference 13% (95% CI 3-23)]. There was not any significant association of menopause age with carotid plaque presence or progression in fully-adjusted models. Conclusion: In a multiethnic cohort, grand multiparity was independently associated with carotid plaque presence and progression. Early menopause, a known risk factor for CVD, was not captured by carotid plaque in this study. These findings may have implications for refining CVD risk assessment in women.
Language	English
Publishing date	2023-08-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2616844-3
ISSN	2160-200X
ISSN	2160-200X
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Article ; Online: Neuronal genetic rescue normalizes brain network dynamics in a lysosomal storage disorder despite persistent storage accumulation.

Ahrens-Nicklas, Rebecca C / Tecedor, Luis / Hall, Arron F / Kane, Owen / Chung, Richard J / Lysenko, Elena / Marsh, Eric D / Stein, Colleen S / Davidson, Beverly L

Molecular therapy : the journal of the American Society of Gene Therapy

2022 Volume 30, Issue 7, Page(s) 2464–2473

Abstract: Although neurologic symptoms occur in two-thirds of lysosomal storage disorders (LSDs), for most we do not understand the mechanisms underlying brain dysfunction. A major unanswered question is if the pathogenic hallmark of LSDs, storage accumulation, ... ...

Abstract	Although neurologic symptoms occur in two-thirds of lysosomal storage disorders (LSDs), for most we do not understand the mechanisms underlying brain dysfunction. A major unanswered question is if the pathogenic hallmark of LSDs, storage accumulation, induces functional defects directly or is a disease bystander. Also, for most LSDs we do not know the impact of loss of function in individual cell types. Understanding these critical questions are essential to therapy development. Here, we determine the impact of genetic rescue in distinct cell types on neural circuit dysfunction in CLN3 disease, the most common pediatric dementia and a paradigmatic neurodegenerative LSD. We restored Cln3 expression via AAV-mediated gene delivery and conditional genetic rescue in a CLN3 disease mouse model. Surprisingly, we found that low-level rescue of Cln3 expression in neurons alone normalized clinically relevant electrophysiologic markers of network dysfunction, despite the presence of substantial residual histopathology, in contrast to restoring expression in astrocytes. Thus, loss of CLN3 function in neurons, not storage accumulation, underlies neurologic dysfunction in CLN3 disease. This impliesies that storage clearance may be an inappropriate target for therapy development and an ineffectual biomarker.
MeSH term(s)	Animals ; Brain/metabolism ; Child ; Humans ; Lysosomal Storage Diseases/genetics ; Lysosomal Storage Diseases/metabolism ; Lysosomal Storage Diseases/therapy ; Lysosomes/metabolism ; Membrane Glycoproteins/genetics ; Mice ; Molecular Chaperones/genetics ; Neuronal Ceroid-Lipofuscinoses/genetics ; Neuronal Ceroid-Lipofuscinoses/metabolism ; Neuronal Ceroid-Lipofuscinoses/therapy ; Neurons/metabolism
Chemical Substances	CLN3 protein, human ; CLN3 protein, mouse ; Membrane Glycoproteins ; Molecular Chaperones
Language	English
Publishing date	2022-04-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2010592-7
ISSN	1525-0024 ; 1525-0016
ISSN (online)	1525-0024
ISSN	1525-0016
DOI	10.1016/j.ymthe.2022.03.025
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Article ; Online: Taking the body off the mind: Decreased functional connectivity between somatomotor and default-mode networks following Floatation-REST.

Al Zoubi, Obada / Misaki, Masaya / Bodurka, Jerzy / Kuplicki, Rayus / Wohlrab, Colleen / Schoenhals, William A / Refai, Hazem H / Khalsa, Sahib S / Stein, Murray B / Paulus, Martin P / Feinstein, Justin S

Human brain mapping

2021 Volume 42, Issue 10, Page(s) 3216–3227

Abstract: Floatation-Reduced Environmental Stimulation Therapy (REST) is a procedure that reduces stimulation of the human nervous system by minimizing sensory signals from visual, auditory, olfactory, gustatory, thermal, tactile, vestibular, gravitational, and ... ...

Abstract	Floatation-Reduced Environmental Stimulation Therapy (REST) is a procedure that reduces stimulation of the human nervous system by minimizing sensory signals from visual, auditory, olfactory, gustatory, thermal, tactile, vestibular, gravitational, and proprioceptive channels, in addition to minimizing musculoskeletal movement and speech. Initial research has found that Floatation-REST can elicit short-term reductions in anxiety, depression, and pain, yet little is known about the brain networks impacted by the intervention. This study represents the first functional neuroimaging investigation of Floatation-REST, and we utilized a data-driven exploratory analysis to determine whether the intervention leads to altered patterns of resting-state functional connectivity (rsFC). Healthy participants underwent functional magnetic resonance imaging (fMRI) before and after 90 min of Floatation-REST or a control condition that entailed resting supine in a zero-gravity chair for an equivalent amount of time. Multivariate Distance Matrix Regression (MDMR), a statistically-stringent whole-brain searchlight approach, guided subsequent seed-based connectivity analyses of the resting-state fMRI data. MDMR identified peak clusters of rsFC change between the pre- and post-float fMRI, revealing significant decreases in rsFC both within and between posterior hubs of the default-mode network (DMN) and a large swath of cortical tissue encompassing the primary and secondary somatomotor cortices extending into the posterior insula. The control condition, an active form of REST, showed a similar pattern of reduced rsFC. Thus, reduced stimulation of the nervous system appears to be reflected by reduced rsFC within the brain networks most responsible for creating and mapping our sense of self.
MeSH term(s)	Adolescent ; Adult ; Connectome ; Default Mode Network/diagnostic imaging ; Default Mode Network/physiology ; Female ; Humans ; Hydrotherapy ; Insular Cortex/diagnostic imaging ; Insular Cortex/physiology ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Motor Cortex/diagnostic imaging ; Motor Cortex/physiology ; Nerve Net/diagnostic imaging ; Nerve Net/physiology ; Sensory Deprivation/physiology ; Somatosensory Cortex/diagnostic imaging ; Somatosensory Cortex/physiology ; Young Adult
Language	English
Publishing date	2021-04-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1197207-5
ISSN	1097-0193 ; 1065-9471
ISSN (online)	1097-0193
ISSN	1065-9471
DOI	10.1002/hbm.25429
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Zs.A 4028: Show issues

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Article ; Online: Modulating membrane fluidity corrects Batten disease phenotypes in vitro and in vivo.

Schultz, Mark L / Tecedor, Luis / Lysenko, Elena / Ramachandran, Shyam / Stein, Colleen S / Davidson, Beverly L

Neurobiology of disease

2018 Volume 115, Page(s) 182–193

Abstract: The neuronal ceroid lipofuscinoses are a class of inherited neurodegenerative diseases characterized by the accumulation of autofluorescent storage material. The most common neuronal ceroid lipofuscinosis has juvenile onset with rapid onset blindness and ...

Abstract	The neuronal ceroid lipofuscinoses are a class of inherited neurodegenerative diseases characterized by the accumulation of autofluorescent storage material. The most common neuronal ceroid lipofuscinosis has juvenile onset with rapid onset blindness and progressive degeneration of cognitive processes. The juvenile form is caused by mutations in the CLN3 gene, which encodes the protein CLN3. While mouse models of Cln3 deficiency show mild disease phenotypes, it is apparent from patient tissue- and cell-based studies that its loss impacts many cellular processes. Using Cln3 deficient mice, we previously described defects in mouse brain endothelial cells and blood-brain barrier (BBB) permeability. Here we expand on this to other components of the BBB and show that Cln3 deficient mice have increased astrocyte endfeet area. Interestingly, this phenotype is corrected by treatment with a commonly used GAP junction inhibitor, carbenoxolone (CBX). In addition to its action on GAP junctions, CBX has also been proposed to alter lipid microdomains. In this work, we show that CBX modifies lipid microdomains and corrects membrane fluidity alterations in Cln3 deficient endothelial cells, which in turn improves defects in endocytosis, caveolin-1 distribution at the plasma membrane, and Cdc42 activity. In further work using the NIH Library of Integrated Network-based Cellular Signatures (LINCS), we discovered other small molecules whose impact was similar to CBX in that they improved Cln3-deficient cell phenotypes. Moreover, Cln3 deficient mice treated orally with CBX exhibited recovery of impaired BBB responses and reduced autofluorescence. CBX and the compounds identified by LINCS, many of which have been used in humans or approved for other indications, may find therapeutic benefit in children suffering from CLN3 deficiency through mechanisms independent of their original intended use.
MeSH term(s)	Animals ; Cell Line, Transformed ; Female ; Male ; Membrane Fluidity/physiology ; Membrane Glycoproteins/deficiency ; Membrane Glycoproteins/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Molecular Chaperones/genetics ; Neuronal Ceroid-Lipofuscinoses/genetics ; Neuronal Ceroid-Lipofuscinoses/metabolism ; Neuronal Ceroid-Lipofuscinoses/pathology ; Phenotype
Chemical Substances	CLN3 protein, mouse ; Membrane Glycoproteins ; Molecular Chaperones
Language	English
Publishing date	2018-04-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2018.04.010
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Article ; Online: Individual and Site-Specific Variation in a Biogeographical Profile of the Coyote Gastrointestinal Microbiota.

Sugden, Scott / St Clair, Colleen Cassady / Stein, Lisa Y

Microbial ecology

2020 Volume 81, Issue 1, Page(s) 240–252

Abstract: Most knowledge of the vertebrate gut microbiota comes from fecal samples; due to difficulties involved in sample collection, the upper intestinal microbiota is poorly understood in wild animals despite its potential to inform broad interpretations about ... ...

Abstract	Most knowledge of the vertebrate gut microbiota comes from fecal samples; due to difficulties involved in sample collection, the upper intestinal microbiota is poorly understood in wild animals despite its potential to inform broad interpretations about host-gut microbe relationships under natural conditions. Here, we used 16S rRNA gene sequencing to characterize the microbiota of wild coyotes (Canis latrans) along the gastrointestinal tract, including samples from the duodenum, jejunum, ileum, caecum, ascending and descending colon, and feces. We used this intestinal profile to (1) quantify how intestinal site and individual identity interact to shape the microbiota in an uncontrolled setting, and (2) evaluate whether the fecal microbiota adequately represent other intestinal sites. Microbial communities in the large intestine were distinct from those in the small intestine, with higher diversity and a greater abundance of anaerobic taxa. Within each of the small and large intestine, individual identity explained significantly more among-sample variation than specific intestinal sites, revealing the importance of individual variation in the microbiota of free-living animals. Fecal samples were not an adequate proxy for studying upper intestinal environments, as they contained only half the amplicon sequence variants (ASVs) present in the small intestine at three- to four-fold higher abundances. Our study is a unique biogeographical investigation of the microbiota using free-living mammals rather than livestock or laboratory organisms and provides a foundational understanding of the gastrointestinal microbiota in a wild canid.
MeSH term(s)	Animals ; Bacteria/classification ; Bacteria/genetics ; Bacteria/isolation & purification ; Coyotes/microbiology ; DNA, Bacterial/genetics ; Feces/microbiology ; Gastrointestinal Microbiome/genetics ; Gastrointestinal Tract/microbiology ; High-Throughput Nucleotide Sequencing ; RNA, Ribosomal, 16S/genetics
Chemical Substances	DNA, Bacterial ; RNA, Ribosomal, 16S
Language	English
Publishing date	2020-06-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	1462065-0
ISSN	1432-184X ; 0095-3628
ISSN (online)	1432-184X
ISSN	0095-3628
DOI	10.1007/s00248-020-01547-0
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