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7. Validity of the Short Weekly Calendar Planning Activity in patients with Parkinson disease and nonmanifesting LRRK2 and GBA carriers

Author

Schejter‐Margalit, Tamara, primary, Binyamin, Noam Ben, additional, Thaler, Avner, additional, Maidan, Inbal, additional, Cedarbaum, Jesse M., additional, Orr‐Urtreger, Avi, additional, Gana Weisz, Mali, additional, Goldstein, Orly, additional, Giladi, Nir, additional, Mirelman, Anat, additional, and Kizony, Rachel, additional

Published
2024
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16. MAPT Locus in Parkinson's Disease Patients of Ashkenazi Origin: A Stratified Analysis.

Author

Shani, Shachar, Gana-Weisz, Mali, Bar-Shira, Anat, Thaler, Avner, Gurevich, Tanya, Mirelman, Anat, Giladi, Nir, Alcalay, Roy N., Goldstein, Orly, and Orr-Urtreger, Avi

Subjects
*GENE expression, *PARKINSON'S disease, *LOCUS (Genetics), *MISSENSE mutation, *GENETIC variation, *WHOLE genome sequencing
Abstract

Introduction: MAPT locus is associated with Parkinson's disease (PD), which is located within a large inversion region of high linkage disequilibrium (LD). We aimed to determine whether the H2-haplotype protective effect and its effect size depends on the GBA1 or LRRK2 risk allele carrier status, and to further characterize genetic alterations that might contribute to its effect. Methods: LD analysis was performed using whole-genome sequencing data of 202 unrelated Ashkenazi Jewish (AJ) PDs. A haplotype-divergent variant was genotyped in a cohort of 1200 consecutively recruited AJ-PDs. The odd ratios were calculated using AJ-non-neuro cases from the gnomAD database as the controls in an un-stratified and a stratified manner according to the mutation carrier status, and the effect on the Age at Motor Symptom Onset (AMSO) was examined. Expression and splicing quantitative trait locus (eQTL and sQTL) analyses were carried out using brain tissues from a database. Results: The H2 haplotype exhibited significant association with PD protection, with a similar effect size in GBA1 carriers, LRRK2-G2019S carriers, and non-carriers (OR = 0.77, 0.69, and 0.82, respectively), and there was no effect on AMSO. The LD interval was narrowed to approximately 1.2 Mb. The H2 haplotype carried potential variants in candidate genes (MAPT and SPPL2C); structural deletions and segmental duplication (KANSL1); and variants affecting gene expression and intron excision ratio in brain tissues (LRRC37A/2). Conclusions: Our results demonstrate that H2 is associated with PD and its protective effect is not influenced by the GBA1/LRRK2 risk allele carrier status. This effect may be genetically complex, resulting from different levels of variations such as missense mutations in relevant genes, structural variations, epigenetic modifications, and RNA expression changes, which may operate independently or in synergy. [ABSTRACT FROM AUTHOR]

Published
2024
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19. The influence of GBA and LRRK2 on mood disorders in Parkinson's Disease

Author

DeBroff, Jake, primary, Omer, Nurit, additional, Cohen, Batsheva, additional, Giladi, Nir, additional, Kestenbaum, Meir, additional, Shirvan, Julia C., additional, Cedarbaum, Jesse M., additional, Gana‐Weisz, Mali, additional, Goldstein, Orly, additional, Orr‐Urtreger, Avi, additional, Mirelman, Anat, additional, and Thaler, Avner, additional

Published
2023
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20. Genetic markers of Restless Legs Syndrome in Parkinson disease

Author

Gan-Or, Ziv, Alcalay, Roy N., Bar-Shira, Anat, Leblond, Claire S., Postuma, Ronald B., Ben-Shachar, Shay, Waters, Cheryl, Johnson, Amelie, Levy, Oren, Mirelman, Anat, Gana-Weisz, Mali, Dupré, Nicolas, Montplaisir, Jacques, Giladi, Nir, Fahn, Stanley, Xiong, Lan, Dion, Patrick A., Orr-Urtreger, Avi, and Rouleau, Guy A.

Published
2015
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21. The natural history study of preclinical genetic Creutzfeldt-Jakob Disease (CJD): A prospective longitudinal study protocol

Author

Bregman Noa, Shiner Tamara, Kavé Gitit, Alcalay Roy, Gana-Weisz Mali, Goldstein Orly, Glinka Tal, Aizenstein Orna, Ben Bashat Dafna, Alcalay Yifat, Mirelman Anat, Thaler Avner, Giladi Nir, and Omer Nurit

Subjects
Neurology (clinical), General Medicine
Abstract

Background Creutzfeldt-Jakob Disease (CJD) is the most common prion disease in humans causing a rapidly progressive neurological decline and dementia and is invariably fatal. The familial forms (genetic CJD, gCJD) are caused by mutations in the PRNP gene encoding for the prion protein (PrP). In Israel, there is a large cluster of gCJD cases, carriers of an E200K mutation in the PRNP gene, and therefore the largest population of at-risk individuals in the world. The mutation is not necessarily sufficient for the formation and accumulation of the pathological prion protein (PrPsc), suggesting that other, genetic and non-genetic factors affect the age at symptoms onset. Here we present the protocol of a cross-sectional and longitudinal natural history study of gCJD patients and first-degree relatives of gCJD patients, aiming to identify biological markers of preclinical CJD and risk factors for phenoconversion. Methods The study has two groups: Patients diagnosed with gCJD, and first-degree healthy relatives (HR) (both carriers and non-carriers of the E200K mutation in the PRNP gene) of patients diagnosed with gCJD. At baseline, and at the end of every year, healthy participants are invited for an “in-depth” visit, which includes a clinical evaluation, blood and urine collection, gait assessment, brain MRI, lumbar puncture (LP), and Polysomnography (PSG). At 6 months from baseline, and then halfway through each year, participants are invited for a “brief” visit, which includes a clinical evaluation, short cognitive assessment, and blood and urine collection. gCJD patients will be invited for one “in-depth” visit, similar to the baseline visit of healthy relatives. Discussion This continuous follow-up of the participants and the frequent assessments will allow early identification and diagnosis in case of conversion into disease. The knowledge generated from this study is likely to advance the understanding of the underlying clinicopathological processes that occur at the very beginning of CJD, as well as potential genetic and environmental risk factors for the development of the disease, therefore advancing the development of safe and efficient interventions. Trial registration The study is an observational study. It has registered retrospectively in https://clinicaltrials.gov/ and has been assigned an identification number NCT05746715.

Published
2022
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25. Requirement of ATM-Dependent Monoubiquitylation of Histone H2B for Timely Repair of DNA Double-Strand Breaks

Author

Moyal, Lilach, Lerenthal, Yaniv, Gana-Weisz, Mali, Mass, Gilad, So, Sairei, Wang, Shih-Ya, Eppink, Berina, Chung, Young Min, Shalev, Gil, Shema, Efrat, Shkedy, Dganit, Smorodinsky, Nechama I., van Vliet, Nicole, Kuster, Bernhard, Mann, Matthias, Ciechanover, Aaron, Dahm-Daphi, Jochen, Kanaar, Roland, Hu, Mickey C.-T., Chen, David J., Oren, Moshe, and Shiloh, Yosef

Published
2011
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26. Glucocerebrosidase Activity Is Not Associated with Parkinson's Disease Risk or Severity

Author

Omer, Nurit, primary, Giladi, Nir, additional, Gurevich, Tanya, additional, Bar‐Shira, Anat, additional, Gana‐Weisz, Mali, additional, Glinka, Tal, additional, Goldstein, Orly, additional, Kestenbaum, Meir, additional, Cedarbaum, Jesse M., additional, Mabrouk, Omar S., additional, Fraser, Kyle B., additional, Shirvan, Julia C., additional, Orr‐Urtreger, Avi, additional, Mirelman, Anat, additional, and Thaler, Avner, additional

Published
2022
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27. <italic>P2RX7,</italic> an adaptive immune response gene, is associated with Parkinson's disease risk and age at onset.

Author

Shani, Shachar, Gana-Weisz, Mali, Bar-Shira, Anat, Thaler, Avner, Gurevich, Tanya, Mirelman, Anat, Giladi, Nir, Alcalay, Roy N., Orr-Urtreger, Avi, and Goldstein, Orly

Subjects
*AGE of onset, *PARKINSON'S disease, *PURINERGIC receptors, *GENETIC variation, *SUBSTANTIA nigra
Abstract

\n The adaptive immune response has a role in Parkinson's disease (PD). Patients with LRRK2 or GBA1 mutations often exhibit distinct clinical characteristics.To evaluate the involvement of adaptive immune response genes in three PD groups: GBA1-PD, LRRK2-PD, and non-carrier (NC)-PD.Differentially expressed genes (DEGs) associated with PD were identified using four datasets. Of them, adaptive immune response genes were evaluated using whole-genome-sequencing of 201 unrelated Ashkenazi-Jewish (AJ) PD patients. Potential pathogenic variants were identified, and P2RX7 variants were assessed in 1200 AJ-PD patients. Burden analysis of rare variants (allele frequencies (AF) < 0.01) on disease risk, and association analyses of common variants (AF ≥ 0.01) with disease risk and age-at-onset (AAO) were conducted. AFs were compared to AJ-non-neuro cases reported in gnomAD. Variants associated with PD were further examined in an independent AJ cohort from AMP-PD.Of the four adaptive immune DEGs identified, CD8B2, P2RX7, IL27RA, and ZC3H12A, three common variants in P2RX7 were statistically significant: Tyr155His was associated with NC-PD (allelic OR = 1.15, p = 0.015) ; Arg276His was associated with LRRK2-PD (allelic OR = 2.10, p = 0.037), while Glu496Ala was associated with earlier AAO in LRRK2-PD (p = 0.014). Burden analysis showed no significant effect on PD-risk. In the AMP-PD cohort, odds ratios of the two risk variants were similar to the primary cohort, but did not reach significance, probably due to small control sample size (n = 263).Common variants within P2RX7 are likely associated with PD-risk and earlier AAO. These findings further suggest P2RX7's involvement in PD and its potential interplay with LRRK2.Plain Language Summary: Among many causes, evidence suggest that the immune system plays a role in the development of Parkinson's disease (PD). This study focused on understanding how certain immune-related genes might be involved in PD risk, including people who carry already known genetic risk mutations in LRRK2 and GBA1 genes. Four genes related to the adaptive immune response, CD8B2, P2RX7, IL27RA, and ZC3H12A, demonstrated different expression in the substantia nigra (a primary brain region of neuronal loss in PD) between PD patients and healthy individuals. We focused on P2RX7 (Purinergic Receptor P2X 7) gene and examined the potential enrichment of its genetic variations in a large group of 1200 PD patients of Ashkenazi-Jewish origin, compared to healthy individuals, which may suggest genetic involvement in the disease. Three common DNA variations in this gene were found to be associated with PD. Two of them were linked to a higher risk of PD, and another one was linked to an earlier disease onset in patients who carry a LRRK2 mutation. P2RX7 activation has been linked to inflammation. Our results suggest that this gene could play a role in PD development, which may lead to new approaches for treatment and prevention. [ABSTRACT FROM AUTHOR]

Published
2024
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28. C9orf72-G4C2 Intermediate Repeats and Parkinson’s Disease

Author

Kobo, Hila, Goldstein, Orly, Gana-Weisz, Mali, Bar-Shira, Anat, Gurevich, Tanya, Thaler, Avner, Mirelman, Anat, Giladi, Nir, and Orr-Urtreger, Avi

Subjects
hexanucleotide expansions, C9orf72, mental disorders, intermediate repeats, nutritional and metabolic diseases, Parkinson’s disease (PD), nervous system diseases
Abstract

Pathogenic C9orf72-G4C2 repeat expansions are associated with ALS/FTD, but not with Parkinson’s disease (PD), yet the possible link between intermediate repeat lengths and PD remains inconclusive. We aim to study the potential involvement of these repeats in PD. The number of C9orf72-repeats were determined by flanking and repeat-primed PCR assays, and the risk-haplotype was determined by SNP-array. Their association with PD was assessed in a stratified manner: in PD-patients-carriers of mutations in LRRK2, GBA, or SMPD1 genes (n = 388), and in PD-non-carriers (NC, n = 718). Allelic distribution was significantly different only in PD-NC compared to 600 controls when looking both at the allele with higher repeat’s size (p = 0.034) and at the combined number of repeats from both alleles (p = 0.023). Intermediate repeats (20–60 repeats) were associated with PD in PD-NC patients (p = 0.041, OR = 3.684 (CI 1.05–13.0)) but not in PD-carriers (p = 0.684). The C9orf72 risk-haplotype, determined in a subgroup of 588 PDs and 126 controls, was observed in higher frequency in PD-NC (dominant model, OR = 1.71, CI 1.04–2.81, p = 0.0356). All 19 alleles within the risk-haplotype were associated with higher C9orf72 RNA levels according to the GTEx database. Based on our data, we suggest a model in which intermediate repeats are a risk factor for PD in non-carriers, driven not only by the number of repeats but also by the variants’ genotypes within the risk-haplotype. Further studies are needed to elucidate this possible role of C9orf72 in PD pathogenesis.

Published
2021
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32. Glucocerebrosidase Activity is not Associated with Parkinson's Disease Risk or Severity

Author

Omer, Nurit, primary, Giladi, Nir, additional, Gurevich, Tanya, additional, Bar‐Shira, Anat, additional, Gana‐Weisz, Mali, additional, Glinka, Tal, additional, Goldstein, Orly, additional, Kestenbaum, Meir, additional, Cedarbaum, Jesse M., additional, Mabrouk, Omar S., additional, Fraser, Kyle B., additional, Shirvan, Julia C., additional, Orr‐Urtreger, Avi, additional, Mirelman, Anat, additional, and Thaler, Avner, additional

Published
2021
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34. Mutations in GBA and LRRK2 Are Not Associated with Increased Inflammatory Markers

Author

Thaler, Avner, primary, Omer, Nurit, additional, Giladi, Nir, additional, Gurevich, Tanya, additional, Bar-Shira, Anat, additional, Gana-Weisz, Mali, additional, Goldstein, Orly, additional, Kestenbaum, Meir, additional, Shirvan, Julia C., additional, Cedarbaum, Jesse M., additional, Orr-Urtreger, Avi, additional, Regev, Keren, additional, Shenhar-Tsarfaty, Shani, additional, and Mirelman, Anat, additional

Published
2021
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35. Genome-wide mapping of IBD segments in an Ashkenazi PD cohort identifies associated haplotypes

Author

Vacic, Vladimir, Ozelius, Laurie J., Clark, Lorraine N., Bar-Shira, Anat, Gana-Weisz, Mali, Gurevich, Tanya, Gusev, Alexander, Kedmi, Merav, Kenny, Eimear E., Liu, Xinmin, Mejia-Santana, Helen, Mirelman, Anat, Raymond, Deborah, Saunders-Pullman, Rachel, Desnick, Robert J., Atzmon, Gil, Burns, Edward R., Ostrer, Harry, Hakonarson, Hakon, Bergman, Aviv, Barzilai, Nir, Darvasi, Ariel, Peter, Inga, Guha, Saurav, Lencz, Todd, Giladi, Nir, Marder, Karen, Peʼer, Itsik, Bressman, Susan B., and Orr-Urtreger, Avi

Published
2014
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37. Parkinson disease phenotype in Ashkenazi jews with and without LRRK2 G2019S mutations

Author

Alcalay, Roy N., Mirelman, Anat, Saunders-Pullman, Rachel, Tang, Ming-X, Mejia Santana, Helen, Raymond, Deborah, Roos, Ernest, Orbe-Reilly, Martha, Gurevich, Tanya, Bar Shira, Anat, Gana Weisz, Mali, Yasinovsky, Kira, Zalis, Maayan, Thaler, Avner, Deik, Andres, Barrett, Matthew James, Cabassa, Jose, Groves, Mark, Hunt, Ann L., Lubarr, Naomi, San Luciano, Marta, Miravite, Joan, Palmese, Christina, Sachdev, Rivka, Sarva, Harini, Severt, Lawrence, Shanker, Vicki, Swan, Matthew Carrington, Soto-Valencia, Jeannie, Johannes, Brooke, Ortega, Robert, Fahn, Stanley, Cote, Lucien, Waters, Cheryl, Mazzoni, Pietro, Ford, Blair, Louis, Elan, Levy, Oren, Rosado, Llency, Ruiz, Diana, Dorovski, Tsvyatko, Pauciulo, Michael, Nichols, William, Orr-Urtreger, Avi, Ozelius, Laurie, Clark, Lorraine, Giladi, Nir, Bressman, Susan, and Marder, Karen S.

Published
2013
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43. A Possible Modifying Effect of the G2019S Mutation in the LRRK2 Gene on GBA Parkinson's Disease.

Author

Omer, Nurit, Giladi, Nir, Gurevich, Tanya, Bar‐Shira, Anat, Gana‐Weisz, Mali, Goldstein, Orly, Kestenbaum, Meir, Cedarbaum, Jesse M., Orr‐Urtreger, Avi, Mirelman, Anat, Thaler, Avner, Bar-Shira, Anat, Gana-Weisz, Mali, and Orr-Urtreger, Avi

Subjects
PARKINSON'S disease & genetics, RESEARCH, GENETIC mutation, RESEARCH methodology, MEDICAL cooperation, EVALUATION research, COMPARATIVE studies, GENOTYPES, GLYCOSIDASES, RESEARCH funding
Abstract

Background: The phenotype of Parkinson's disease (PD) is milder among patients with LRRK2-PD and more severe among patients with GBA-PD; however, whether an additive phenotypical effect occurs among dual-mutation carriers requires validation.Objective: The objective of this study was to explore the phenotypic expression of patients with PD who carry mutations in both genes compared with a single-mutation presentation.Methods: Patients with PD were genotyped for the G2019S-LRRK2 mutation and 9 mutations in the GBA gene. Subjects were classified into 5 groups: idiopathic PD, mild GBA-PD, severe GBA-PD, LRRK2-PD, and LRRK2+GBA-PD. Clinical symptoms were evaluated using performance-based measures.Results: A total of 1090 patients with idiopathic PD, 155 patients with LRRK2-PD, 155 patients with mild GBA-PD, 56 patients with severe GBA-PD, and 27 patients with LRRK2+GBA-PD participated in this study. The patients with LRRK2-PD and LRRK2+GBA-PD exhibited lower scores on total Unified Parkinson's Disease Rating Scale (P < 0.01) and better olfaction (P < 0.01) compared with GBA-PD.Conclusions: Patients with LRRK2+GBA-PD were symptomatically similar to patients with LRRK2-PD, suggesting a dominant effect of LRRK2 over GBA in the phenotypic presentation. © 2020 International Parkinson and Movement Disorder Society. [ABSTRACT FROM AUTHOR]

Published
2020
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44. Application of the Movement Disorder Society Prodromal Criteria in healthy G2019S-LRRK2 carriers

Author

Mirelman, Anat, Saunders-Pullman, Rachel, Alcalay, Roy N, Shustak, Shiran, Thaler, Avner, Gurevich, Tanya, Raymond, Deborah, Mejia-Santana, Helen, Reilly, Martha Orbe, Ozelius, Laurie, Clark, Lorraine, Gana-Weisz, Mali, Bar-Shira, Anat, Orr-Utreger, Avi, Bressman, Susan B, Marder, Karen, and Giladi, Nir

Subjects
Adult, Aged, 80 and over, Male, Movement Disorders, Glycine, Prodromal Symptoms, Middle Aged, Leucine-Rich Repeat Serine-Threonine Protein Kinase-2, Article, Young Adult, Mutation, Serine, Humans, Female, Longitudinal Studies, Societies, Medical, Aged
Abstract

In 2015, the International Parkinson and Movement Disorder Society Task Force recommended research criteria for the estimation of prodromal PD.We aimed to evaluate, for the first time, the criteria in first-degree relatives of Ashkenazi Jewish G2019S-LRRK2 PD patients, who are considered a population at risk for developing PD, and assess the sensitivity and specificity of the criteria in identifying phenoconverters.Participants were evaluated longitudinally over a period of 5 years (average follow-up: 49.2 ± 12.3 months). Likelihood ratios and probability estimations were calculated based on the International Parkinson and Movement Disorder Society Research Criteria for Prodromal Parkinson's Disease markers and examined for each assessment point.One hundred twenty healthy carriers (49.53 ± 13.4 years; 54% female) and 111 healthy noncarriers (48.43 ± 15.79 years; 49% female) participated in this study. Probability scores were significantly higher in healthy carriers than healthy noncarriers (P0.0001). Of the 20 participants (8.6%) who met criteria for probable prodromal PD at baseline, 17 were healthy carriers. Participants who reached the threshold were older (P0.0001), had higher UPDRS-III (P0.001), lower cognitive function (P = 0.001), and more nonmotor symptoms (P0.0001), compared to those who did not. Ten participants were diagnosed with incident PD within 5 years from baseline resulting in a specificity of 91.82% (95% confidence interval: 86.69-96.94), sensitivity of 80% (95% confidence interval: 55.21-100), positive predictive value of 47.06% (95% confidence interval: 23.33-70.79), and negative predictive value of 98.06% (95% confidence interval: 95.39-100). All 10 phenoconvertors were G2019S-LRRK2 carriers.The results showed the utility of using the criteria and high sensitivity and specificity in identifying prodromal PD in this high-risk unique cohort. These results may be valuable for future disease modification clinical trials. © 2018 International Parkinson and Movement Disorder Society.

Published
2018

45. Hierarchical Data-Driven Analysis of Clinical Symptoms Among Patients With Parkinson's Disease

Author

Kozlovski, Tal, primary, Mitelpunkt, Alexis, additional, Thaler, Avner, additional, Gurevich, Tanya, additional, Orr-Urtreger, Avi, additional, Gana-Weisz, Mali, additional, Shachar, Netta, additional, Galili, Tal, additional, Marcus-Kalish, Mira, additional, Bressman, Susan, additional, Marder, Karen, additional, Giladi, Nir, additional, Benjamini, Yoav, additional, and Mirelman, Anat, additional

Published
2019
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46. Mutations in GBAand LRRK2Are Not Associated with Increased Inflammatory Markers

Author

Thaler, Avner, Omer, Nurit, Giladi, Nir, Gurevich, Tanya, Bar-Shira, Anat, Gana-Weisz, Mali, Goldstein, Orly, Kestenbaum, Meir, Shirvan, Julia C., Cedarbaum, Jesse M., Orr-Urtreger, Avi, Regev, Keren, Shenhar-Tsarfaty, Shani, and Mirelman, Anat

Abstract

Inflammation is an integral part of neurodegeneration including in Parkinson’s disease (PD). Ashkenazi Jews have high rates of genetic PD with divergent phenotypes among GBA-PD and LRRK2-PD. The role of inflammation in the prodromal phase of PD and the association with disease phenotype has yet to be elucidated. To assess central and peripheral cytokines among PD patients with mutations in the LRRK2and GBAgenes and among non-manifesting carriers (NMC) of these mutations in order to determine the role of inflammation in genetic PD. The following cytokines were assessed from peripheral blood and cerebrospinal fluid (CSF): TNF-α, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10 and INF- γ. A comprehensive intake including general medical conditions, use of anti-inflammatory treatments, motor and cognitive assessments and additional laboratory measures were recorded, enabling the construction of the MDS probable prodromal score. Data from 362 participants was collected: 31 idiopathic PD (iPD), 30 LRRK2-PD, 77 GBA-PD, 3 homozygote GBA-PD, 3 GBA-LRRK2-PD, 67 LRRK2-NMC, 105 GBA-NMC, 14 LRRK2-GBA-NMC, and 32 healthy controls. No between-group differences in peripheral or CSF cytokines were detected. No correlation between disease characteristics or risk for prodromal PD could be associated with any inflammatory measure. In this study, we could not detect any evidence on dysregulated immune response among GBAand LRRK2PD patients and non-manifesting mutation carriers.

Published
2021
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49. Application of the Movement Disorder Society Prodromal Criteria in healthy G2019S-LRRK2 carriers (S3.002)

Author

Mirelman, Anat, primary, Saunders-Pullman, Rachel, additional, Alcalay, Roy, additional, Shustak, Shiran, additional, Thaler, Avner, additional, Raymond, Deborah, additional, Mejia-Santana, Helen, additional, Reily, Martha Orbe, additional, Ozelius, Laurie, additional, Clark, Lorraine, additional, Gana-Weisz, Mali, additional, Bar-Shira, Anat, additional, Orr-Utreger, Avi, additional, Bressman, Susan, additional, Marder, Karen, additional, and Giladi, Nir, additional

Published
2018
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