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The complexity of branching and curvilinear morphology of a complete mitochondrial network within each cell is challenging to analyze and quantify. To address this challenge, we developed an image analysis technique using persistent homology with a multiparameter filtration framework, combining image processing techniques in mathematical morphology. We show that such filtrations contain both topological and geometric information about complex cellular organelle structures, which allows a software program to extract meaningful features. Using this information, we also develop a connectivity index that describes the morphology of the branching patterns. As proof of concept, we utilize this approach to study how mitochondrial networks are altered by genetic changes in the Optineurin gene. Mutations in the autophagy gene Optineurin (OPTN) are associated with primary open-angle glaucoma (POAG), amyotrophic lateral sclerosis (ALS), and Paget's disease of the bone, but the pathophysiological mechanism is unclear. We utilized the proposed mathematical morphology-based multiparameter filtration and persistent homology approach to analyze and quantitatively compare how changes in the OPTN gene alter mitochondrial structures from their normal interconnected, tubular morphology into scattered, fragmented pieces., Competing Interests: NO authors have competing interests., (Copyright: © 2024 Chung et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Estimating the nutritional requirements for pediatric patients requires a comprehensive approach with various factors including age, gender, body mass index, and physical activity level, due to the significant growth and developmental changes observed in this population. This complexity renders the use of a simplistic generalization or a standard formula impractical. A number of methodologies have been established to calculate nutritional needs for the pediatric population. However, the application of these methodologies is challenging due to the variability in the aforementioned factors. Determining nutritional requirements for pediatric patients with underlying medical conditions is complicate, influenced by variables such as the nature of the illness, treatment modalities, and the patient's overall condition. Nutritional support in severely traumatically brain-injured pediatric patients is directly correlated with prognosis and growth outcomes. Therefore, this case study aims to validate existing methodologies for estimating nutritional requirements in pediatric patients with severe traumatic brain injury and to provide primary data for the development of effective nutritional support strategies. A case of a 5-year-old male patient admitted to the intensive care unit due to severe traumatic brain injury is examined. Future case studies and ongoing research are imperative to ensure the safe and effective nutritional support of pediatric patients with severe traumatic brain injury., Competing Interests: Conflict of Interest: The authors declare that they have no competing interests., (Copyright © 2024. The Korean Society of Clinical Nutrition.)

Progression of prostate cancer depends on androgen receptor, which is usually activated by androgens. Therefore, a mainstay treatment is androgen deprivation therapy. Unfortunately, despite initial treatment response, resistance nearly always develops, and disease progresses to castration-resistant prostate cancer (CRPC), which remains driven by non-gonadal androgens synthesized in prostate cancer tissues. 3β-Hydroxysteroid dehydrogenase/Δ 5 -->4 isomerase 1 (3βHSD1) catalyzes the rate-limiting step in androgen synthesis. However, how 3βHSD1, especially the "adrenal-permissive" 3βHSD1(367T) that permits tumor synthesis of androgen from dehydroepiandrosterone (DHEA), is regulated at the protein level is not well understood. Here, we investigate how hypoxia regulates 3βHSD1(367T) protein levels. Our results show that, in vitro, hypoxia stabilizes 3βHSD1 protein by suppressing autophagy. Autophagy inhibition promotes 3βHSD1-dependent tumor progression. Hypoxia represses transcription of autophagy-related (ATG) genes by decreasing histone acetylation. Inhibiting deacetylase (HDAC) restores ATG gene transcription under hypoxia. Therefore, HDAC inhibition may be a therapeutic target for hypoxic tumor cells., Competing Interests: Declaration of interests N.S. reports grants from BMS and grants from Astellas outside the submitted work; in addition, N.S. has a patent for HSD3B1 in prostate cancer issued., (Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved.)