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2. Choledochal stenting for treatment of extrahepatic biliary obstruction in cats

Author

Griffin, Maureen A, Culp, William TN, Giuffrida, Michelle A, Selmic, Laura E, Denitz, Jordan C, Perry, James A, Schoelkopf, Alexander C, Milovancev, Milan, Phillips, Heidi, Wallace, Mandy L, Steffey, Michele A, Balsa, Ingrid M, and Mayhew, Philipp D

Subjects
Veterinary Sciences, Agricultural, Veterinary and Food Sciences, Assistive Technology, Bioengineering, Digestive Diseases, Animals, Cat Diseases, Cats, Cholestasis, Extrahepatic, Retrospective Studies, Stents, Treatment Outcome, bilirubin, common bile duct, gallbladder, icterus, stent, Veterinary sciences
Abstract

BackgroundLimited information currently exists regarding the clinical progression and outcomes of cats that undergo choledochal stenting as a treatment for extrahepatic biliary obstruction (EHBO).Hypothesis/objectivesDescribe clinical characteristics, indications for choledochal stent placement, procedure, and outcomes in a cohort of cats undergoing choledochal stenting and evaluate risk factors associated with survival as well as recurrence of EHBO in affected cats.AnimalsTwenty-three client-owned cats undergoing choledochal stent placement.MethodsRetrospective study. Medical records from 6 academic institutions were reviewed, and data were extracted and analyzed statistically.ResultsMedian age of cats was 10.1 years (range, 2-16), and all cats had at least 2 clinical signs. Most common clinical signs were vomiting in 20/22 (90.9%), inappetence in 19/22 (86.4%), and lethargy in 19/23 (82.6%). Procedural complications were uncommon and rarely related to the stenting procedure. Clinical signs improved postoperatively in 15/20 (75.0%) cats and serum total bilirubin concentration decreased postoperatively in 13/19 (68.4%) cats. Eighteen (78.3%) cats survived to discharge. Recurrence of EHBO was documented in 7/18 (38.9%) cats that survived to discharge. Cholelithiasis was associated with recurrence of EHBO. Median survival time for cats that survived to discharge was 931 days (range, 19-3034). Absence of peritoneal effusion was associated with survival to discharge.Conclusions and clinical importanceCholedochal stenting was an effective treatment modality in cats with EHBO with few procedural complications and potential for prolonged survival, but substantial risk for recurrence of EHBO was identified.

Published
2021

4. Autophagy suppression in DNA damaged cells occurs through a newly identified p53-proteasome-LC3 axis

Author

Lieu, D’Feau J., primary, Crowder, Molly K., additional, Kryza, Jordan R., additional, Tamilselvam, Batcha, additional, Kaminski, Paul J., additional, Kim, Ik-Jung, additional, Li, Yingxing, additional, Jeong, Eunji, additional, Enkhbaatar, Michidmaa, additional, Chen, Henry, additional, Son, Sophia B., additional, Mok, Hanlin, additional, Bradley, Kenneth A., additional, Phillips, Heidi, additional, and Blanke, Steven R., additional

Published
2024
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5. Clinical findings, diagnostic test results, and treatment outcome in cats with hiatal hernia: 31 cases (1995‐2018)

Author

Phillips, Heidi, Corrie, Jessica, Engel, Danielle M, Duffy, Daniel J, Holt, David E, Kendall, Allison R, Schmiedt, Chad W, Vetter, Autumn, Meren, Ilyssa L, Follette, Christelle, Schaeffer, David J, Mayhew, Philipp D, and Marks, Stanley L

Subjects
Veterinary Sciences, Agricultural, Veterinary and Food Sciences, Digestive Diseases, Rare Diseases, Animals, Cat Diseases, Cats, Comorbidity, Female, Hernia, Hiatal, Male, Retrospective Studies, Treatment Outcome, esophagopexy, gastroesophageal junction, gastropexy, phrenoplasty, reflux esophagitis, Veterinary sciences
Abstract

BackgroundInformation regarding clinical signs, assessment, treatment, and outcome in cats with hiatal hernia (HH) is limited.ObjectivesTo characterize the clinical presentation of HH and medical and surgical outcomes in a cohort of affected cats.AnimalsThirty-one client-owned cats with HH.MethodsMedical records of cats with HH were retrospectively reviewed for signalment, history, results of diagnostic tests, details of surgical and medical treatments, complications, and outcome. Long-term follow-up data were obtained by telephone communication. Relationships between clinical variables and outcome were evaluated by regression analysis.ResultsType I HH was present in 85.7% (24/28) of cats, and 64.5% (20/31) were >3 years of age at diagnosis. Twenty-one of 31 (67.7%) cats underwent surgical repair including phrenoplasty, esophagopexy, and left-sided gastropexy, and 10 of 31 cats were treated medically without surgery. Concurrent illness was common, and 77.4% cats had comorbidities. All cats survived to discharge, and median time to death or follow-up was 959 days (range, 3-4015 days). Cats treated medically survived longer than cats treated surgically, with median time to death or follow-up of 2559 and 771 days, respectively.Conclusions and clinical importanceType I HH is the most common type of HH in cats. A congenital etiology is possible, but many cats with HH were >3 years of age at diagnosis and suffered from comorbidities, including upper airway obstruction. Case selection and the presence of comorbidities likely influenced the outcome. Cats with HH may not be diagnosed until disease is advanced or concurrent illness draws attention to clinical signs.

Published
2019

6. METABOLIC PATHWAYS

Author

Blough, Michael, Al-Najjar, Mohammad, Stechishin, Owen, Ronen, Sabrina, Weiss, Samuel, Luchman, H, Cairncross, J, Fonkem, Ekokobe, Tobin, Richard, Griffin, Jennifer, Zuzek, Alex, Rogers, Martha, Kathagen, Annegret, Schulte, Alexander, Balcke, Gerd, Phillips, Heidi, Günther, Hauke, Westphal, Manfred, Lamszus, Katrin, Fack, Fred, Bonnel, David, Hochart, Guillaume, Navis, Anna, Wesseling, Pieter, Leenders, William, Stauber, Jonathan, Niclou, Simone, Sahm, Felix, Oezen, Iris, Opitz, Christiane, Radlwimmer, Bernhard, von Deimling, Andreas, Bode, Helge, Ahrendt, Tilman, Adams, Seray, Guillemin, Gilles, Wick, Wolfgang, Platten, Michael, Vartanian, Alenoush, Singh, Sanjay, Burrell, Kelly, Agnihotri, Sameer, Sabha, Nesrin, Zadeh, Gelareh, Teo, Charles, McDonald, Kerrie, Zinger, Anna, Bustamante, Sonia, Lim, Chai, Braidy, Nady, Brew, Bruce, Wolf, Amparo, Lang, Fredrick, Verhaak, Roel, Hawkins, Cynthia, Aldape, Kenneth, Chesnelong, Charles, and Chaumeil, Myriam

Abstract

The kynurenine pathway (KP) is the principal route of L-Tryptophan (TRP) catabolism leading to the production of kynurenine (KYN), the neuroprotectants, kynurenic acid (KYNA) and picolinic acid (PIC), and the excitotoxic neurotoxin, quinolinic acid (QUIN). The enzymes indoleamine 2,3-dioxygenase-1 (IDO-1), indoleamine 2, 3-dioxygenase-2 (IDO-2) and tryptophan 2,3-dioxygenase (TDO-2) initiate the first step of the KP. Downstream enzymes include kynureninase (KYNU), 3-hydroxyanthranilate 3,4-dioxygenase (3-HAAO), kynurenine hydroxylase (KMO) and 2-amino-3-carboxymuconate semialdehyde decarboxylase (ACMSD). Kynurenine aminotransferase-I (KAT-I) is one of the enzymes responsible for synthesising KYNA. Mounting evidence directly implicates that IDO-1 induction in various tumours is a crucial mechanism facilitating tumour immune evasion and persistence. However, the involvement of the downstream machinery of the KP in brain tumour progression remains unexplored. A complete characterisation of the KP in brain tumours and the role of the KP in maintaining homeostasis between neuroprotection and neurodegeneration in glioma has not yet been investigated. Here we report the first comprehensive characterisation of the KP in cultured human glioma cells and GBM patient plasma. Our qRT-PCR data revealed that interferon-gamma (IFN-γ) (100 IU/ml) stimulation significantly potentiated the expression of IDO-1 IDO-2, KYNU, 3-HAAO, KMO and significantly down-regulated ACMSD and KAT-I expression in cultured human glioma cells. HPLC analysis revealed that IFN-γ stimulation significantly increased KP activity (KYN/TRP ratio), and significantly lowered the KYNA/KYN neuroprotective ratio in human cultured glioma cells. Our HPLC and GCMS data revealed that KP activation was significantly higher and the concentrations of TRP, KYNA, QUIN and PIC and the KYNA/KYN ratio were significantly lower in GBM patient plasma (n = 18) compared to controls. These results provide further evidence for the involvement of the KP in glioma pathophysiology and highlights a potential role of KP products as novel and highly attractive therapeutic targets to evaluate for the treatment of brain tumours.

Published
2013

7. PDGFRA Amplification is Common in Pediatric and Adult High‐Grade Astrocytomas and Identifies a Poor Prognostic Group in IDH1 Mutant Glioblastoma

Author

Phillips, Joanna J, Aranda, Derick, Ellison, David W, Judkins, Alexander R, Croul, Sidney E, Brat, Daniel J, Ligon, Keith L, Horbinski, Craig, Venneti, Sriram, Zadeh, Gelareh, Santi, Mariarita, Zhou, Shengmei, Appin, Christina L, Sioletic, Stefano, Sullivan, Lisa M, Martinez‐Lage, Maria, Robinson, Aaron E, Yong, William H, Cloughesy, Timothy, Lai, Albert, Phillips, Heidi S, Marshall, Roxanne, Mueller, Sabine, Haas‐Kogan, Daphne A, Molinaro, Annette M, and Perry, Arie

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Brain Cancer, Neurosciences, Rare Diseases, Pediatric, Brain Disorders, Genetics, Adolescent, Adult, Astrocytoma, Brain Neoplasms, Child, Child, Preschool, Cohort Studies, DNA Copy Number Variations, Female, Glioblastoma, Humans, Isocitrate Dehydrogenase, Male, Middle Aged, Mutation, Receptor, Platelet-Derived Growth Factor alpha, Sex Factors, Statistics, Nonparametric, Young Adult, astrocytoma, FISH, IDH1, isocitrate dehydrogenase 1, PDGFRA, prognosis, Clinical Sciences, Neurology & Neurosurgery, Clinical sciences
Abstract

High-grade astrocytomas (HGAs), corresponding to World Health Organization grades III (anaplastic astrocytoma) and IV (glioblastoma; GBM), are biologically aggressive, and their molecular classification is increasingly relevant to clinical management. PDGFRA amplification is common in HGAs, although its prognostic significance remains unclear. Using fluorescence in situ hybridization (FISH), the most sensitive technique for detecting PDGFRA copy number gains, we determined PDGFRA amplification status in 123 pediatric and 263 adult HGAs. A range of PDGFRA FISH patterns were identified and cases were scored as non-amplified (normal and polysomy) or amplified (low-level and high-level). PDGFRA amplification was frequent in pediatric (29.3%) and adult (20.9%) tumors. Amplification was not prognostic in pediatric HGAs. In adult tumors diagnosed initially as GBM, the presence of combined PDGFRA amplification and isocitrate dehydrogenase 1 (IDH1)(R132H) mutation was a significant independent prognostic factor (P = 0.01). In HGAs, PDGFRA amplification is common and can manifest as high-level and focal or low-level amplifications. Our data indicate that the latter is more prevalent than previously reported with copy number averaging techniques. To our knowledge, this is the largest survey of PDGFRA status in adult and pediatric HGAs and suggests PDGFRA amplification increases with grade and is associated with a less favorable prognosis in IDH1 mutant de novo GBMs.

Published
2013

8. Identifying the mesenchymal molecular subtype of glioblastoma using quantitative volumetric analysis of anatomic magnetic resonance images

Author

Naeini, Kourosh M, Pope, Whitney B, Cloughesy, Timothy F, Harris, Robert J, Lai, Albert, Eskin, Ascia, Chowdhury, Reshmi, Phillips, Heidi S, Nghiemphu, Phioanh L, Behbahanian, Yalda, and Ellingson, Benjamin M

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Neurosciences, Brain Cancer, Cancer, Genetics, Rare Diseases, Brain Disorders, Biomarkers, Tumor, Brain Neoplasms, Clinical Trials, Phase II as Topic, Contrast Media, Follow-Up Studies, Glioblastoma, Humans, Magnetic Resonance Imaging, Mesoderm, Necrosis, Prognosis, Retrospective Studies, Tumor Burden, GBM, glioblastoma, IDH1, mesenchymal, molecular subtypes, MRI, radiogenomics, Oncology and Carcinogenesis, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

BackgroundSubtypes of glioblastoma multiforme (GBM) based on genetic and molecular alterations are thought to cause alterations in anatomic MRI owing to downstream biological changes, such as edema production, blood-brain barrier breakdown, and necrosis. The purpose of the current study was to identify a potential relationship between imaging features and the mesenchymal (MES) GBM subtype, which has the worst patient prognosis.MethodsMRIs from 46 patients with histologically confirmed GBM were retrospectively analyzed. The volume of contrast enhancement, regions of central necrosis, and hyperintensity of T2/fluid attenuated inversion recovery (FLAIR) were measured. Additionally, the ratio of T2/FLAIR hyperintense volume to the volume of contrast enhancement and necrosis was calculated.ResultsThe volume of contrast enhancement, volume of central necrosis, combined volume of contrast enhancement and central necrosis, and the ratio of T2/FLAIR to contrast enhancement and necrosis were significantly different in MES compared with non-MES GBM (Mann-Whitney, P < .05). Receiver-operator characteristics indicated that these 4 metrics were all significant predictors of the MES phenotype. The volume ratio of T2 hyperintensity to contrast enhancement and central necrosis was significantly lower in MES vs non-MES GBM (P < .0001), was a significant predictor of the MES phenotype (area under the curve = 0.93, P < .001), and could be used to stratify short- and long-term overall survival (log-rank, P = .0064 using cutoff of 3.0). These trends were also present when excluding isocitrate dehydrogenase 1 mutant tumors and incorporating covariates such as age and KPS score.ConclusionsResults suggest that volume ratio may be a simple, cost-effective, and noninvasive biomarker for quickly identifying MES GBM.

Published
2013

9. Anatomic localization of O6-methylguanine DNA methyltransferase (MGMT) promoter methylated and unmethylated tumors: A radiographic study in 358 de novo human glioblastomas

Author

Ellingson, Benjamin M, Cloughesy, Timothy F, Pope, Whitney B, Zaw, Taryar M, Phillips, Heidi, Lalezari, Shadi, Nghiemphu, Phioanh L, Ibrahim, Hassana, Naeini, Kourosh M, Harris, Robert J, and Lai, Albert

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Neurosciences, Cancer, Brain Cancer, Genetics, Brain Disorders, Rare Diseases, Brain, Brain Neoplasms, DNA Methylation, DNA Modification Methylases, DNA Repair Enzymes, Female, Glioblastoma, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Promoter Regions, Genetic, Tissue Distribution, Tumor Suppressor Proteins, Radiogenomics, MGMT, GBM, Tumor location, Medical and Health Sciences, Psychology and Cognitive Sciences, Neurology & Neurosurgery, Biomedical and clinical sciences, Health sciences
Abstract

Promoter methylation of O6-methylguanine DNA methyltransferase (MGMT) is associated with a favorable prognosis in glioblastoma multiforme (GBM) and has been hypothesized to occur early in tumor transformation of glial cells. Thus, a possible link exists between the site of malignant transformation and MGMT promoter methylation status. Using the Analysis of Differential Involvement (ADIFFI) statistical mapping technique in a total of 358 patients with GBM, we demonstrate that human de novo GBMs occur in a high frequency contiguous with the posterior subventricular zone (SVZ); MGMT promoter methylated GBMs are lateralized to the left hemisphere, while MGMT unmethylated GBMs are lateralized to the right hemisphere; and tumors near the left temporal lobe have a significantly longer overall survival compared with tumors occurring elsewhere, independent of treatment or MGMT methylation status.

Published
2012

12. Supplementary Figure 3 from Identification and Analysis of In Vivo VEGF Downstream Markers Link VEGF Pathway Activity with Efficacy of Anti-VEGF Therapies

Author

Brauer, Matthew J., primary, Zhuang, Guanglei, primary, Schmidt, Maike, primary, Yao, Jenny, primary, Wu, Xiumin, primary, Kaminker, Joshua S., primary, Jurinka, Stefanie S., primary, Kolumam, Ganesh, primary, Chung, Alicia S., primary, Jubb, Adrian, primary, Modrusan, Zora, primary, Ozawa, Tomoko, primary, James, C. David, primary, Phillips, Heidi, primary, Haley, Benjamin, primary, Tam, Rachel N.W., primary, Clermont, Anne C., primary, Cheng, Jason H., primary, Yang, Sherry X., primary, Swain, Sandra M., primary, Chen, Daniel, primary, Scherer, Stefan J., primary, Koeppen, Hartmut, primary, Yeh, Ru-Fang, primary, Yue, Peng, primary, Stephan, Jean-Philippe, primary, Hegde, Priti, primary, Ferrara, Napoleone, primary, Singh, Mallika, primary, and Bais, Carlos, primary

Published
2023
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14. Supplementary Figure 1 from Identification and Analysis of In Vivo VEGF Downstream Markers Link VEGF Pathway Activity with Efficacy of Anti-VEGF Therapies

Author

Brauer, Matthew J., primary, Zhuang, Guanglei, primary, Schmidt, Maike, primary, Yao, Jenny, primary, Wu, Xiumin, primary, Kaminker, Joshua S., primary, Jurinka, Stefanie S., primary, Kolumam, Ganesh, primary, Chung, Alicia S., primary, Jubb, Adrian, primary, Modrusan, Zora, primary, Ozawa, Tomoko, primary, James, C. David, primary, Phillips, Heidi, primary, Haley, Benjamin, primary, Tam, Rachel N.W., primary, Clermont, Anne C., primary, Cheng, Jason H., primary, Yang, Sherry X., primary, Swain, Sandra M., primary, Chen, Daniel, primary, Scherer, Stefan J., primary, Koeppen, Hartmut, primary, Yeh, Ru-Fang, primary, Yue, Peng, primary, Stephan, Jean-Philippe, primary, Hegde, Priti, primary, Ferrara, Napoleone, primary, Singh, Mallika, primary, and Bais, Carlos, primary

Published
2023
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15. Supplementary Methods, Tables 1 - 3 from Identification and Analysis of In Vivo VEGF Downstream Markers Link VEGF Pathway Activity with Efficacy of Anti-VEGF Therapies

Author

Brauer, Matthew J., primary, Zhuang, Guanglei, primary, Schmidt, Maike, primary, Yao, Jenny, primary, Wu, Xiumin, primary, Kaminker, Joshua S., primary, Jurinka, Stefanie S., primary, Kolumam, Ganesh, primary, Chung, Alicia S., primary, Jubb, Adrian, primary, Modrusan, Zora, primary, Ozawa, Tomoko, primary, James, C. David, primary, Phillips, Heidi, primary, Haley, Benjamin, primary, Tam, Rachel N.W., primary, Clermont, Anne C., primary, Cheng, Jason H., primary, Yang, Sherry X., primary, Swain, Sandra M., primary, Chen, Daniel, primary, Scherer, Stefan J., primary, Koeppen, Hartmut, primary, Yeh, Ru-Fang, primary, Yue, Peng, primary, Stephan, Jean-Philippe, primary, Hegde, Priti, primary, Ferrara, Napoleone, primary, Singh, Mallika, primary, and Bais, Carlos, primary

Published
2023
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16. Supplementary Table 1 from Targeting the PI3K Pathway in the Brain—Efficacy of a PI3K Inhibitor Optimized to Cross the Blood–Brain Barrier

Author

Salphati, Laurent, primary, Heffron, Timothy P., primary, Alicke, Bruno, primary, Nishimura, Merry, primary, Barck, Kai, primary, Carano, Richard A., primary, Cheong, Jonathan, primary, Edgar, Kyle A., primary, Greve, Joan, primary, Kharbanda, Samir, primary, Koeppen, Hartmut, primary, Lau, Shari, primary, Lee, Leslie B., primary, Pang, Jodie, primary, Plise, Emile G., primary, Pokorny, Jenny L., primary, Reslan, Hani Bou, primary, Sarkaria, Jann N., primary, Wallin, Jeffrey J., primary, Zhang, Xiaolin, primary, Gould, Stephen E., primary, Olivero, Alan G., primary, and Phillips, Heidi S., primary

Published
2023
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17. Supplementary Figure 2 from Identification and Analysis of In Vivo VEGF Downstream Markers Link VEGF Pathway Activity with Efficacy of Anti-VEGF Therapies

Author

Brauer, Matthew J., primary, Zhuang, Guanglei, primary, Schmidt, Maike, primary, Yao, Jenny, primary, Wu, Xiumin, primary, Kaminker, Joshua S., primary, Jurinka, Stefanie S., primary, Kolumam, Ganesh, primary, Chung, Alicia S., primary, Jubb, Adrian, primary, Modrusan, Zora, primary, Ozawa, Tomoko, primary, James, C. David, primary, Phillips, Heidi, primary, Haley, Benjamin, primary, Tam, Rachel N.W., primary, Clermont, Anne C., primary, Cheng, Jason H., primary, Yang, Sherry X., primary, Swain, Sandra M., primary, Chen, Daniel, primary, Scherer, Stefan J., primary, Koeppen, Hartmut, primary, Yeh, Ru-Fang, primary, Yue, Peng, primary, Stephan, Jean-Philippe, primary, Hegde, Priti, primary, Ferrara, Napoleone, primary, Singh, Mallika, primary, and Bais, Carlos, primary

Published
2023
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18. Supplementary Figure Legend from Targeting the PI3K Pathway in the Brain—Efficacy of a PI3K Inhibitor Optimized to Cross the Blood–Brain Barrier

Author

Salphati, Laurent, primary, Heffron, Timothy P., primary, Alicke, Bruno, primary, Nishimura, Merry, primary, Barck, Kai, primary, Carano, Richard A., primary, Cheong, Jonathan, primary, Edgar, Kyle A., primary, Greve, Joan, primary, Kharbanda, Samir, primary, Koeppen, Hartmut, primary, Lau, Shari, primary, Lee, Leslie B., primary, Pang, Jodie, primary, Plise, Emile G., primary, Pokorny, Jenny L., primary, Reslan, Hani Bou, primary, Sarkaria, Jann N., primary, Wallin, Jeffrey J., primary, Zhang, Xiaolin, primary, Gould, Stephen E., primary, Olivero, Alan G., primary, and Phillips, Heidi S., primary

Published
2023
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19. Supplementary Figure 6 from Identification and Analysis of In Vivo VEGF Downstream Markers Link VEGF Pathway Activity with Efficacy of Anti-VEGF Therapies

Author

Brauer, Matthew J., primary, Zhuang, Guanglei, primary, Schmidt, Maike, primary, Yao, Jenny, primary, Wu, Xiumin, primary, Kaminker, Joshua S., primary, Jurinka, Stefanie S., primary, Kolumam, Ganesh, primary, Chung, Alicia S., primary, Jubb, Adrian, primary, Modrusan, Zora, primary, Ozawa, Tomoko, primary, James, C. David, primary, Phillips, Heidi, primary, Haley, Benjamin, primary, Tam, Rachel N.W., primary, Clermont, Anne C., primary, Cheng, Jason H., primary, Yang, Sherry X., primary, Swain, Sandra M., primary, Chen, Daniel, primary, Scherer, Stefan J., primary, Koeppen, Hartmut, primary, Yeh, Ru-Fang, primary, Yue, Peng, primary, Stephan, Jean-Philippe, primary, Hegde, Priti, primary, Ferrara, Napoleone, primary, Singh, Mallika, primary, and Bais, Carlos, primary

Published
2023
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20. Supplementary Figure 2 from Targeting the PI3K Pathway in the Brain—Efficacy of a PI3K Inhibitor Optimized to Cross the Blood–Brain Barrier

Author

Salphati, Laurent, primary, Heffron, Timothy P., primary, Alicke, Bruno, primary, Nishimura, Merry, primary, Barck, Kai, primary, Carano, Richard A., primary, Cheong, Jonathan, primary, Edgar, Kyle A., primary, Greve, Joan, primary, Kharbanda, Samir, primary, Koeppen, Hartmut, primary, Lau, Shari, primary, Lee, Leslie B., primary, Pang, Jodie, primary, Plise, Emile G., primary, Pokorny, Jenny L., primary, Reslan, Hani Bou, primary, Sarkaria, Jann N., primary, Wallin, Jeffrey J., primary, Zhang, Xiaolin, primary, Gould, Stephen E., primary, Olivero, Alan G., primary, and Phillips, Heidi S., primary

Published
2023
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22. Supplementary Table 4 from Targeting the PI3K Pathway in the Brain—Efficacy of a PI3K Inhibitor Optimized to Cross the Blood–Brain Barrier

Author

Salphati, Laurent, primary, Heffron, Timothy P., primary, Alicke, Bruno, primary, Nishimura, Merry, primary, Barck, Kai, primary, Carano, Richard A., primary, Cheong, Jonathan, primary, Edgar, Kyle A., primary, Greve, Joan, primary, Kharbanda, Samir, primary, Koeppen, Hartmut, primary, Lau, Shari, primary, Lee, Leslie B., primary, Pang, Jodie, primary, Plise, Emile G., primary, Pokorny, Jenny L., primary, Reslan, Hani Bou, primary, Sarkaria, Jann N., primary, Wallin, Jeffrey J., primary, Zhang, Xiaolin, primary, Gould, Stephen E., primary, Olivero, Alan G., primary, and Phillips, Heidi S., primary

Published
2023
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23. Supplementary Figure 1 from Targeting the PI3K Pathway in the Brain—Efficacy of a PI3K Inhibitor Optimized to Cross the Blood–Brain Barrier

Author

Salphati, Laurent, primary, Heffron, Timothy P., primary, Alicke, Bruno, primary, Nishimura, Merry, primary, Barck, Kai, primary, Carano, Richard A., primary, Cheong, Jonathan, primary, Edgar, Kyle A., primary, Greve, Joan, primary, Kharbanda, Samir, primary, Koeppen, Hartmut, primary, Lau, Shari, primary, Lee, Leslie B., primary, Pang, Jodie, primary, Plise, Emile G., primary, Pokorny, Jenny L., primary, Reslan, Hani Bou, primary, Sarkaria, Jann N., primary, Wallin, Jeffrey J., primary, Zhang, Xiaolin, primary, Gould, Stephen E., primary, Olivero, Alan G., primary, and Phillips, Heidi S., primary

Published
2023
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24. Supplementary Figure 5 from Identification and Analysis of In Vivo VEGF Downstream Markers Link VEGF Pathway Activity with Efficacy of Anti-VEGF Therapies

Author

Brauer, Matthew J., primary, Zhuang, Guanglei, primary, Schmidt, Maike, primary, Yao, Jenny, primary, Wu, Xiumin, primary, Kaminker, Joshua S., primary, Jurinka, Stefanie S., primary, Kolumam, Ganesh, primary, Chung, Alicia S., primary, Jubb, Adrian, primary, Modrusan, Zora, primary, Ozawa, Tomoko, primary, James, C. David, primary, Phillips, Heidi, primary, Haley, Benjamin, primary, Tam, Rachel N.W., primary, Clermont, Anne C., primary, Cheng, Jason H., primary, Yang, Sherry X., primary, Swain, Sandra M., primary, Chen, Daniel, primary, Scherer, Stefan J., primary, Koeppen, Hartmut, primary, Yeh, Ru-Fang, primary, Yue, Peng, primary, Stephan, Jean-Philippe, primary, Hegde, Priti, primary, Ferrara, Napoleone, primary, Singh, Mallika, primary, and Bais, Carlos, primary

Published
2023
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25. Supplementary Table 3 from Targeting the PI3K Pathway in the Brain—Efficacy of a PI3K Inhibitor Optimized to Cross the Blood–Brain Barrier

Author

Salphati, Laurent, primary, Heffron, Timothy P., primary, Alicke, Bruno, primary, Nishimura, Merry, primary, Barck, Kai, primary, Carano, Richard A., primary, Cheong, Jonathan, primary, Edgar, Kyle A., primary, Greve, Joan, primary, Kharbanda, Samir, primary, Koeppen, Hartmut, primary, Lau, Shari, primary, Lee, Leslie B., primary, Pang, Jodie, primary, Plise, Emile G., primary, Pokorny, Jenny L., primary, Reslan, Hani Bou, primary, Sarkaria, Jann N., primary, Wallin, Jeffrey J., primary, Zhang, Xiaolin, primary, Gould, Stephen E., primary, Olivero, Alan G., primary, and Phillips, Heidi S., primary

Published
2023
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26. Supplementary Figure 4 from Identification and Analysis of In Vivo VEGF Downstream Markers Link VEGF Pathway Activity with Efficacy of Anti-VEGF Therapies

Author

Brauer, Matthew J., primary, Zhuang, Guanglei, primary, Schmidt, Maike, primary, Yao, Jenny, primary, Wu, Xiumin, primary, Kaminker, Joshua S., primary, Jurinka, Stefanie S., primary, Kolumam, Ganesh, primary, Chung, Alicia S., primary, Jubb, Adrian, primary, Modrusan, Zora, primary, Ozawa, Tomoko, primary, James, C. David, primary, Phillips, Heidi, primary, Haley, Benjamin, primary, Tam, Rachel N.W., primary, Clermont, Anne C., primary, Cheng, Jason H., primary, Yang, Sherry X., primary, Swain, Sandra M., primary, Chen, Daniel, primary, Scherer, Stefan J., primary, Koeppen, Hartmut, primary, Yeh, Ru-Fang, primary, Yue, Peng, primary, Stephan, Jean-Philippe, primary, Hegde, Priti, primary, Ferrara, Napoleone, primary, Singh, Mallika, primary, and Bais, Carlos, primary

Published
2023
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27. Supplementary Table 2 from Targeting the PI3K Pathway in the Brain—Efficacy of a PI3K Inhibitor Optimized to Cross the Blood–Brain Barrier

Author

Salphati, Laurent, primary, Heffron, Timothy P., primary, Alicke, Bruno, primary, Nishimura, Merry, primary, Barck, Kai, primary, Carano, Richard A., primary, Cheong, Jonathan, primary, Edgar, Kyle A., primary, Greve, Joan, primary, Kharbanda, Samir, primary, Koeppen, Hartmut, primary, Lau, Shari, primary, Lee, Leslie B., primary, Pang, Jodie, primary, Plise, Emile G., primary, Pokorny, Jenny L., primary, Reslan, Hani Bou, primary, Sarkaria, Jann N., primary, Wallin, Jeffrey J., primary, Zhang, Xiaolin, primary, Gould, Stephen E., primary, Olivero, Alan G., primary, and Phillips, Heidi S., primary

Published
2023
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28. Data from Reversing HOXA9 Oncogene Activation by PI3K Inhibition: Epigenetic Mechanism and Prognostic Significance in Human Glioblastoma

Author

Costa, Bruno M., primary, Smith, Justin S., primary, Chen, Ying, primary, Chen, Justin, primary, Phillips, Heidi S., primary, Aldape, Kenneth D., primary, Zardo, Giuseppe, primary, Nigro, Janice, primary, James, C. David, primary, Fridlyand, Jane, primary, Reis, Rui M., primary, and Costello, Joseph F., primary

Published
2023
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29. Supplementary Table 2 from Reversing HOXA9 Oncogene Activation by PI3K Inhibition: Epigenetic Mechanism and Prognostic Significance in Human Glioblastoma

Author

Costa, Bruno M., primary, Smith, Justin S., primary, Chen, Ying, primary, Chen, Justin, primary, Phillips, Heidi S., primary, Aldape, Kenneth D., primary, Zardo, Giuseppe, primary, Nigro, Janice, primary, James, C. David, primary, Fridlyand, Jane, primary, Reis, Rui M., primary, and Costello, Joseph F., primary

Published
2023
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30. Supplementary Table 5 from Reversing HOXA9 Oncogene Activation by PI3K Inhibition: Epigenetic Mechanism and Prognostic Significance in Human Glioblastoma

Author

Costa, Bruno M., primary, Smith, Justin S., primary, Chen, Ying, primary, Chen, Justin, primary, Phillips, Heidi S., primary, Aldape, Kenneth D., primary, Zardo, Giuseppe, primary, Nigro, Janice, primary, James, C. David, primary, Fridlyand, Jane, primary, Reis, Rui M., primary, and Costello, Joseph F., primary

Published
2023
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31. Supplementary Table 4 from Reversing HOXA9 Oncogene Activation by PI3K Inhibition: Epigenetic Mechanism and Prognostic Significance in Human Glioblastoma

Author

Costa, Bruno M., primary, Smith, Justin S., primary, Chen, Ying, primary, Chen, Justin, primary, Phillips, Heidi S., primary, Aldape, Kenneth D., primary, Zardo, Giuseppe, primary, Nigro, Janice, primary, James, C. David, primary, Fridlyand, Jane, primary, Reis, Rui M., primary, and Costello, Joseph F., primary

Published
2023
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32. Supplementary Table 1 from Reversing HOXA9 Oncogene Activation by PI3K Inhibition: Epigenetic Mechanism and Prognostic Significance in Human Glioblastoma

Author

Costa, Bruno M., primary, Smith, Justin S., primary, Chen, Ying, primary, Chen, Justin, primary, Phillips, Heidi S., primary, Aldape, Kenneth D., primary, Zardo, Giuseppe, primary, Nigro, Janice, primary, James, C. David, primary, Fridlyand, Jane, primary, Reis, Rui M., primary, and Costello, Joseph F., primary

Published
2023
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33. Supplementary Figures 1-7 from Reversing HOXA9 Oncogene Activation by PI3K Inhibition: Epigenetic Mechanism and Prognostic Significance in Human Glioblastoma

Author

Costa, Bruno M., primary, Smith, Justin S., primary, Chen, Ying, primary, Chen, Justin, primary, Phillips, Heidi S., primary, Aldape, Kenneth D., primary, Zardo, Giuseppe, primary, Nigro, Janice, primary, James, C. David, primary, Fridlyand, Jane, primary, Reis, Rui M., primary, and Costello, Joseph F., primary

Published
2023
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34. Supplementary Methods from Reversing HOXA9 Oncogene Activation by PI3K Inhibition: Epigenetic Mechanism and Prognostic Significance in Human Glioblastoma

Author

Costa, Bruno M., primary, Smith, Justin S., primary, Chen, Ying, primary, Chen, Justin, primary, Phillips, Heidi S., primary, Aldape, Kenneth D., primary, Zardo, Giuseppe, primary, Nigro, Janice, primary, James, C. David, primary, Fridlyand, Jane, primary, Reis, Rui M., primary, and Costello, Joseph F., primary

Published
2023
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35. Supplementary Table 3 from Reversing HOXA9 Oncogene Activation by PI3K Inhibition: Epigenetic Mechanism and Prognostic Significance in Human Glioblastoma

Author

Costa, Bruno M., primary, Smith, Justin S., primary, Chen, Ying, primary, Chen, Justin, primary, Phillips, Heidi S., primary, Aldape, Kenneth D., primary, Zardo, Giuseppe, primary, Nigro, Janice, primary, James, C. David, primary, Fridlyand, Jane, primary, Reis, Rui M., primary, and Costello, Joseph F., primary

Published
2023
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40. Reliability in performance assessment creates a potential application of artificial intelligence in veterinary education: evaluation of suturing skills at a single institution.

Author

Kuzminsky, Jennifer, Phillips, Heidi, Sharif, Hajar, Moran, Clara, Gleason, Hadley E., Topulos, Sophia P., Pitt, Kathryn, McNeil, Leslie Klis, McCoy, Annette M., and Kesavadas, Thenkurussi

Subjects
*SUTURES, *VETERINARY medicine education, *ARTIFICIAL intelligence, *MACHINE learning, *ASSESSMENT of education, *SUTURING
Abstract

OBJECTIVES To evaluate suturing skills of veterinary students using 3 common performance assessments (PAs) and to compare findings to data obtained by an electromyographic armband. SAMPLE 16 second-year veterinary students. PROCEDURES Students performed 4 suturing tasks on synthetic tissue models 1, 3, and 5 weeks after a surgical skills course. Digital videos were scored by 4 expert surgeons using 3 PAs (an Objective Structured Clinical Examination [OSCE]- style surgical binary checklist, an Objective Structured Assessment of Technical Skill [OSATS] checklist, and a surgical Global Rating Scale [GRS]). Surface electromyography (sEMG) data collected from the dominant forearm were input to machine learning algorithms. Performance assessment scores were compared between experts and correlated to task completion times and sEMG data. Inter-rater reliability was calculated using the intraclass correlation coefficient (ICC). Inter-rater agreement was calculated using percent agreement with varying levels of tolerance. RESULTS Reliability was moderate for the OSCE and OSATS checklists and poor for the GRS. Agreement was achieved for the checklists when moderate tolerance was applied but remained poor for the GRS. sEMG signals did not correlate well with checklist scores or task times, but features extracted from signals permitted task differentiation by routine statistical comparison and correct task classification using machine learning algorithms. CLINICAL RELEVANCE Reliability and agreement of an OSCE-style checklist, OSATS checklist, and surgical GRS assessment were insufficient to characterize suturing skills of veterinary students. To avoid subjectivity associated with PA by raters, further study of kinematics and EMG data is warranted in the surgical skills evaluation of veterinary students. [ABSTRACT FROM AUTHOR]

Published
2023
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