Submit to Biomedicines Review for Biomedicines

Journal Menu

Journal Browser

► Journal Browser

Biomedicines, Volume 12, Issue 9 (September 2024) – 5 articles

Issues are regarded as officially published after their release is announced to the table of contents alert mailing list.
You may sign up for e-mail alerts to receive table of contents of newly released issues.
PDF is the official format for papers published in both, html and pdf forms. To view the papers in pdf format, click on the "PDF Full-text" link, and use the free Adobe Reader to open them.

Order results

Result details

Section

Show export options Show export options

Select all

Export citation of selected articles as:

23 pages, 3087 KiB

Open AccessReview

Animal Models of Retinopathy of Prematurity: Advances and Metabolic Regulators

by Meenakshi Maurya, Chi-Hsiu Liu, Kiran Bora, Neetu Kushwah, Madeline C. Pavlovich, Zhongxiao Wang and Jing Chen

Biomedicines 2024, 12(9), 1937; https://doi.org/10.3390/biomedicines12091937 (registering DOI) - 23 Aug 2024

Abstract

Retinopathy of prematurity (ROP) is a primary cause of visual impairment and blindness in premature newborns, characterized by vascular abnormalities in the developing retina, with microvascular alteration, neovascularization, and in the most severe cases retinal detachment. To elucidate the pathophysiology and develop therapeutics for ROP, several pre-clinical experimental models of ROP were developed in different species. Among them, the oxygen-induced retinopathy (OIR) mouse model has gained the most popularity and critically contributed to our current understanding of pathological retinal angiogenesis and the discovery of potential anti-angiogenic therapies. A deeper comprehension of molecular regulators of OIR such as hypoxia-inducible growth factors including vascular endothelial growth factors as primary perpetrators and other new metabolic modulators such as lipids and amino acids influencing pathological retinal angiogenesis is also emerging, indicating possible targets for treatment strategies. This review delves into the historical progressions that gave rise to the modern OIR models with a focus on the mouse model. It also reviews the fundamental principles of OIR, recent advances in its automated assessment, and a selected summary of metabolic investigation enabled by OIR models including amino acid transport and metabolism. Full article

(This article belongs to the Special Issue Angiogenesis)

► Show Figures

Figure 1

20 pages, 1674 KiB

Open AccessReview

Decoding Pulmonary Embolism: Pathophysiology, Diagnosis, and Treatment

by Miriam Peracaula, Laura Sebastian, Iria Francisco, Marc Bonnin Vilaplana, Diego A. Rodríguez-Chiaradía and Olga Tura-Ceide

Biomedicines 2024, 12(9), 1936; https://doi.org/10.3390/biomedicines12091936 (registering DOI) - 23 Aug 2024

Abstract

Pulmonary Embolism (PE) is a life-threatening condition initiated by the presence of blood clots in the pulmonary arteries, leading to severe morbidity and mortality. Underlying mechanisms involve endothelial dysfunction, including impaired blood flow regulation, a pro-thrombotic state, inflammation, heightened oxidative stress, and altered vascular remodeling. These mechanisms contribute to vascular diseases stemming from PE, such as recurrent thromboembolism, chronic thromboembolic pulmonary hypertension, post-thrombotic syndrome, right heart failure, and cardiogenic shock. Detailing key risk factors and utilizing hemodynamic stability-based categorization, the review aims for precise risk stratification by applying established diagnostic tools and scoring systems. This article explores both conventional and emerging biomarkers as potential diagnostic tools. Additionally, by synthesizing existing knowledge, it provides a comprehensive outlook of the current enhanced PE management and preventive strategies. The conclusion underscores the need for future research to improve diagnostic accuracy and therapeutic effectiveness in PE. Full article

(This article belongs to the Special Issue Role of Endothelial Cells in Cardiovascular Disease)

► Show Figures

Figure 1

10 pages, 727 KiB

Open AccessArticle

Serum Uric Acid as an Indicator of Right Ventricular Dysfunction in LVAD Patients: A Preliminary Study

by Tomasz Urbanowicz, Małgorzata Tomaszewska, Anna Olasińska-Wiśniewska, Jędrzej Sikora, Ewa Straburzyńska-Migaj, Jakub Piecek, Maksymilian Białasik-Misiorny, Aleksandra Krasińska-Płachta, Andrzej Tykarski and Marek Jemielity

Biomedicines 2024, 12(9), 1935; https://doi.org/10.3390/biomedicines12091935 (registering DOI) - 23 Aug 2024

Viewed by 76

Abstract

(1) Background: Left ventricular assist devices (LVADs) represent mechanical support in end-stage congestive heart failure and are characterized by satisfactory long-term results. Uric acid (UA) represents one of the early heart failure markers whose usefulness was postulated in clinical practice. (2) Methods: Twenty-nine male patients with a median age of 58 (51–62) years were referred for LVAD implantation due to end-stage congestive heart failure in the mean (SD) New York Heart Association (NYHA) status class 3.3 (0.6). Preoperative and postoperative right ventricular (RV) characteristics were compared with serum uric acid concentration within 12 (8–15) months following the implantation. (3) Results: Significant correlations between postoperative uric acid concentration and right ventricular dimension (r = 0.604, p = 0.005), tricuspid annulus plane systolic excursion (TAPSE) (r = −0.496, p = 0.022), left ventricular ejection fraction (r = −0.463, p = 0.046), and N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) (r = 0.505, p = 0.041) were noted. (4) Conclusions: The analysis shows the association between the postoperative RV diameter and TAPSE results in LVAD patients and uric acid concentration. Serum uric acid can be regarded as a possible right ventricular dysfunction marker in LVAD patients. Full article

(This article belongs to the Section Molecular and Translational Medicine)

► Show Figures

Figure 1

33 pages, 4179 KiB

Open AccessArticle

Analysis of Sigma-1 Receptor Antagonist BD1047 Effect on Upregulating Proteins in HIV-1-Infected Macrophages Exposed to Cocaine Using Quantitative Proteomics

by Omar Vélez-López, Kelvin Carrasquillo-Carrión, Yadira M. Cantres-Rosario, Eraysy Machín-Martínez, Manuel E. Álvarez-Ríos, Abiel Roche-Lima, Eduardo L. Tosado-Rodríguez and Loyda M. Meléndez

Biomedicines 2024, 12(9), 1934; https://doi.org/10.3390/biomedicines12091934 (registering DOI) - 23 Aug 2024

Viewed by 199

Abstract

HIV-1 infects monocyte-derived macrophages (MDM) that migrate into the brain and secrete virus and neurotoxic molecules, including cathepsin B (CATB), causing cognitive dysfunction. Cocaine potentiates CATB secretion and neurotoxicity in HIV-infected MDM. Pretreatment with BD1047, a sigma-1 receptor antagonist, before cocaine exposure reduces HIV-1, CATB secretion, and neuronal apoptosis. We aimed to elucidate the intracellular pathways modulated by BD1047 in HIV-infected MDM exposed to cocaine. We hypothesized that the Sig1R antagonist BD1047, prior to cocaine, significantly deregulates proteins and pathways involved in HIV-1 replication and CATB secretion that lead to neurotoxicity. MDM culture lysates from HIV-1-infected women treated with BD1047 before cocaine were compared with untreated controls using TMT quantitative proteomics, bioinformatics, Lima statistics, and pathway analyses. Results demonstrate that pretreatment with BD1047 before cocaine dysregulated eighty (80) proteins when compared with the infected cocaine group. We found fifteen (15) proteins related to HIV-1 infection, CATB, and mitochondrial function. Upregulated proteins were related to oxidative phosphorylation (SLC25A-31), mitochondria (ATP5PD), ion transport (VDAC2–3), endoplasmic reticulum transport (PHB, TMED10, CANX), and cytoskeleton remodeling (TUB1A-C, ANXA1). BD1047 treatment protects HIV-1-infected MDM exposed to cocaine by upregulating proteins that reduce mitochondrial damage, ER transport, and exocytosis associated with CATB-induced neurotoxicity. Full article

(This article belongs to the Special Issue Sigma-1 Receptor in Health and Disease)

► Show Figures

Figure 1

13 pages, 4002 KiB

Open AccessArticle

Calcium-Enhanced Medium-Based Delivery of Splice Modulating Antisense Oligonucleotides in 2D and 3D hiPSC-Derived Neuronal Models

by Ronald A. M. Buijsen, Linda M. van der Graaf, Elsa C. Kuijper, Barry A. Pepers, Elena Daoutsali, Lotte Weel, Vered Raz, David A. Parfitt and Willeke M. C. van Roon-Mom

Biomedicines 2024, 12(9), 1933; https://doi.org/10.3390/biomedicines12091933 (registering DOI) - 23 Aug 2024

Viewed by 166

Abstract

Antisense technology demonstrates significant potential for addressing inherited brain diseases, with over a dozen products already available and numerous others in the development pipeline. The versatility of differentiating induced pluripotent stem cells (iPSCs) into nearly all neural cell types proves invaluable for comprehending the mechanisms behind neurological diseases, replicating cellular phenotypes, and advancing the testing and development of new therapies, including antisense oligonucleotide therapeutics. While delivering antisense oligonucleotides (ASOs) to human iPSC-based neuronal models has posed challenges, this study explores various delivery methods, including lipid-based transfection, gymnotic uptake, Ca⁽²⁺⁾-enhanced medium (CEM)-based delivery, and electroporation, in 2D and 3D hiPSC-derived neuronal models. This study reveals that CEM-based delivery exhibits efficiency and low toxicity in both 2D neuronal cultures and 3D brain organoids. Furthermore, the findings indicate that CEM is slightly more effective in neurons than in astrocytes, suggesting promising avenues for further exploration and optimization of preclinical ASO strategies in the treatment of neurological disorders. Full article

(This article belongs to the Special Issue Applications of 3D Cell Culture in Biomedicines)

► Show Figures