6 results on '"Zeccola, AM"'
Search Results
2. Effect of Age and Prior Gynecologic Surgery on Pathologic Diagnosis in Patients Undergoing Benign Hysterectomy
- Author
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Zeccola, AM, primary, Rindos, NB, additional, and Foley, CE, additional
- Published
- 2019
- Full Text
- View/download PDF
3. Structural and Genetic Studies Demonstrate Neurologic Dysfunction in Triosephosphate Isomerase Deficiency Is Associated with Impaired Synaptic Vesicle Dynamics
- Author
-
Roland, BP, Zeccola, AM, Larsen, SB, Amrich, CG, Talsma, AD, Stuchul, KA, Heroux, A, Levitan, ES, VanDemark, AP, Palladino, MJ, Roland, BP, Zeccola, AM, Larsen, SB, Amrich, CG, Talsma, AD, Stuchul, KA, Heroux, A, Levitan, ES, VanDemark, AP, and Palladino, MJ
- Abstract
Triosephosphate isomerase (TPI) deficiency is a poorly understood disease characterized by hemolytic anemia, cardiomyopathy, neurologic dysfunction, and early death. TPI deficiency is one of a group of diseases known as glycolytic enzymopathies, but is unique for its severe patient neuropathology and early mortality. The disease is caused by missense mutations and dysfunction in the glycolytic enzyme, TPI. Previous studies have detailed structural and catalytic changes elicited by disease-associated TPI substitutions, and samples of patient erythrocytes have yielded insight into patient hemolytic anemia; however, the neuropathophysiology of this disease remains a mystery. This study combines structural, biochemical, and genetic approaches to demonstrate that perturbations of the TPI dimer interface are sufficient to elicit TPI deficiency neuropathogenesis. The present study demonstrates that neurologic dysfunction resulting from TPI deficiency is characterized by synaptic vesicle dysfunction, and can be attenuated with catalytically inactive TPI. Collectively, our findings are the first to identify, to our knowledge, a functional synaptic defect in TPI deficiency derived from molecular changes in the TPI dimer interface.
- Published
- 2016
4. Effect of Patient Age on Decisional Regret After Laparoscopic Hysterectomy.
- Author
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King NR, Zeccola AM, Wang L, Harris JA, and Foley CE
- Subjects
- Humans, Female, Middle Aged, Adult, Retrospective Studies, Age Factors, Surveys and Questionnaires, Hysterectomy psychology, Hysterectomy adverse effects, Laparoscopy psychology, Emotions, Decision Making
- Abstract
Objective: To compare long-term decision regret between younger (30 years or younger) and older (31-49 years) patients who underwent laparoscopic hysterectomy for benign disease., Methods: We conducted a matched retrospective cohort study to analyze patients who underwent laparoscopic hysterectomies for benign indications from 2009 to 2016. Respondents completed surveys including two validated decision regret scales: one measuring surgical decision regret and the other measuring loss-of-fertility regret. Participant aged was dichotomized as 30 years or younger and 31-49 years. Chi square, Fisher exact, and Wilcoxon rank sum tests and logistic regression were used to compare groups., Results: Two hundred eighty-seven participants were successfully contacted, and 241 completed the survey (84.0%). Seventy-seven respondents (32.0%) were aged 30 years or younger, and 164 (68.0%) were aged 31-49 years. The average time since surgery was 7.2 years (±2.2 years; range 3.7-12.1 years). Participants aged 30 years or younger regretted both undergoing surgery (32.5% vs 9.1%, P<.001; OR 4.8, 95% CI, 2.3-9.8) and loss of fertility (39.0% vs 13.4%, P<.001, OR 4.1, 95% CI, 2.2-7.8) at significantly higher rates than participants aged 31-49 years. Overall, 83.1% of younger participants agreed that hysterectomy was the right choice compared with 97% of older participants (P<.001). Higher rates of surgical and loss-of-fertility regret were seen in participants with self-reported pelvic pain (P=.003, P=.011), preoperative diagnosis of endometriosis (P=.037, P=.046), and postoperative complications (P=.043, P<.001). Although time since hysterectomy did not affect rate of surgical regret (P=.138), participants further from their hysterectomies had lower rates of loss-of-fertility regret (P=.003). Patient age remained significantly associated with both surgical regret (adjusted OR 2.9 (95% CI, 1.3-6.5) and loss-of-fertility regret (adjusted OR 2.8 (95% CI, 1.3-6.0) on multivariable logistic regression., Conclusion: Participants aged 30 years or younger were more likely to regret their decision to undergo hysterectomy than participants aged 31-49 years, regardless of parity, prior sterilization, or previous treatment., Competing Interests: Financial Disclosure John A. Harris disclosed the following: The Agency for Healthcare Research and Quality, current, paid to my institution, 1R01HS026943; National Institute of Child Health and Human Development, current, paid to my institution, 1R01HD105712; National Institute of Child Health and Human Development, current, paid to my institution, 1R01HD111038; National Institute on Disability, Independent Living, and Rehabilitation Research, current, paid to my institution, 90DPHF0011; Pennsylvania Department of Health, current, paid to my institution, 4100088553; Lewin Group, past, paid to me, honorarium related to disability health education presentation; University of Kentucky, past, paid to me, honorarium related to disability health education presentation; Colorado Department of Public Health and Environment, past, paid to me, honorarium related to disability health education presentation; University of Missouri, past, paid to me, honorarium related to disability health education presentation; Milestone Pennsylvania, past, paid to me, honorarium related to disability health education presentation; Novo Nordisk, past, paid to me, consulting on Virtual Advisory Board on Women's Health and Obesity Management. The other authors did not report any potential conflicts of interest., (Copyright © 2024 by the American College of Obstetricians and Gynecologists. Published by Wolters Kluwer Health, Inc. All rights reserved.)
- Published
- 2024
- Full Text
- View/download PDF
5. Alternative treatments of adenomyosis - an update in procedural management and clinical outcomes.
- Author
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Zeccola AM and Allen SE
- Subjects
- Humans, Female, Treatment Outcome, High-Intensity Focused Ultrasound Ablation, Dysmenorrhea therapy, Dysmenorrhea etiology, Radiofrequency Ablation methods, Uterine Hemorrhage therapy, Uterine Hemorrhage etiology, Pelvic Pain therapy, Pelvic Pain etiology, Adenomyosis therapy, Uterine Artery Embolization
- Abstract
Purpose of Review: Adenomyosis is a common cause of abnormal uterine bleeding (AUB), dysmenorrhea, and pelvic pain. Definitive diagnosis and treatment have historically been by uterine histopathology at time of hysterectomy; however, advances in imaging have supported earlier diagnosis and subsequent conservative treatment. This review aims to update the evidence supporting the uterine-sparing, procedural management options with a focus on clinical outcomes., Recent Findings: Uterine artery embolization (UAE), radiofrequency ablation (RFA), high-intensity focused ultrasound (HIFU), percutaneous microwave ablation (PMWA), and adenomyomectomy are minimally invasive interventions proven to be effective in reducing AUB and dysmenorrhea due to adenomyosis. Symptom improvement is associated with a decrease in uterine volume. Studies support the use of alternative treatment options given the overall low rates of symptom recurrence and reintervention. Combination therapy may be more effective than monotherapy., Summary: This review provides the current evidence for use of alternative treatment options for adenomyosis. Access to ablative therapies in the USA is limited and primarily off label, given lack of FDA approval. High-quality prospective and randomized controlled trials are needed in order to further delineate treatment comparisons, efficacy, safety, and ideal patient selection for these treatments. More data are needed to assess safety and utility in those desiring future fertility., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)
- Published
- 2024
- Full Text
- View/download PDF
6. Structural and Genetic Studies Demonstrate Neurologic Dysfunction in Triosephosphate Isomerase Deficiency Is Associated with Impaired Synaptic Vesicle Dynamics.
- Author
-
Roland BP, Zeccola AM, Larsen SB, Amrich CG, Talsma AD, Stuchul KA, Heroux A, Levitan ES, VanDemark AP, and Palladino MJ
- Subjects
- Anemia, Hemolytic, Congenital Nonspherocytic pathology, Animals, Behavior, Animal, Carbohydrate Metabolism, Inborn Errors pathology, Crystallography, X-Ray, Dimerization, Humans, Mutation, Missense, Nervous System Diseases pathology, Protein Conformation, Synaptic Vesicles pathology, Triose-Phosphate Isomerase chemistry, Triose-Phosphate Isomerase metabolism, Anemia, Hemolytic, Congenital Nonspherocytic genetics, Carbohydrate Metabolism, Inborn Errors genetics, Drosophila melanogaster genetics, Nervous System Diseases genetics, Synaptic Vesicles genetics, Triose-Phosphate Isomerase deficiency, Triose-Phosphate Isomerase genetics
- Abstract
Triosephosphate isomerase (TPI) deficiency is a poorly understood disease characterized by hemolytic anemia, cardiomyopathy, neurologic dysfunction, and early death. TPI deficiency is one of a group of diseases known as glycolytic enzymopathies, but is unique for its severe patient neuropathology and early mortality. The disease is caused by missense mutations and dysfunction in the glycolytic enzyme, TPI. Previous studies have detailed structural and catalytic changes elicited by disease-associated TPI substitutions, and samples of patient erythrocytes have yielded insight into patient hemolytic anemia; however, the neuropathophysiology of this disease remains a mystery. This study combines structural, biochemical, and genetic approaches to demonstrate that perturbations of the TPI dimer interface are sufficient to elicit TPI deficiency neuropathogenesis. The present study demonstrates that neurologic dysfunction resulting from TPI deficiency is characterized by synaptic vesicle dysfunction, and can be attenuated with catalytically inactive TPI. Collectively, our findings are the first to identify, to our knowledge, a functional synaptic defect in TPI deficiency derived from molecular changes in the TPI dimer interface.
- Published
- 2016
- Full Text
- View/download PDF
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