Journal Description
Biomedicines
Biomedicines
is an international, peer-reviewed, open access journal on biomedicines published monthly online by MDPI. The Society for Regenerative Medicine (Russian Federation) (RPO) is affiliated with Biomedicines and its members receive discounts on the article processing charges.
- Open Access— free for readers, with article processing charges (APC) paid by authors or their institutions.
- High Visibility: indexed within Scopus, SCIE (Web of Science), PubMed, PMC, CAPlus / SciFinder, and other databases.
- Journal Rank: JCR - Q1 (Pharmacology & Pharmacy) / CiteScore - Q2 (Medicine (miscellaneous))
- Rapid Publication: manuscripts are peer-reviewed and a first decision is provided to authors approximately 15.4 days after submission; acceptance to publication is undertaken in 2.9 days (median values for papers published in this journal in the second half of 2023).
- Recognition of Reviewers: reviewers who provide timely, thorough peer-review reports receive vouchers entitling them to a discount on the APC of their next publication in any MDPI journal, in appreciation of the work done.
- Companion journals for Biomedicines include: IJTM, BioMed, Anesthesia Research and Emergency Care and Medicine.
Impact Factor:
4.7 (2022);
5-Year Impact Factor:
4.9 (2022)
Latest Articles
Prognostic Function and Immunologic Landscape of a Predictive Model Based on Five Senescence-Related Genes in IPF Bronchoalveolar Lavage Fluid
Biomedicines 2024, 12(6), 1246; https://doi.org/10.3390/biomedicines12061246 - 3 Jun 2024
Abstract
Background: Idiopathic pulmonary fibrosis (IPF) is a type of interstitial lung disease characterized by unknown causes and a poor prognosis. Recent research indicates that age-related mechanisms, such as cellular senescence, may play a role in the development of this condition. However, the relationship
[...] Read more.
Background: Idiopathic pulmonary fibrosis (IPF) is a type of interstitial lung disease characterized by unknown causes and a poor prognosis. Recent research indicates that age-related mechanisms, such as cellular senescence, may play a role in the development of this condition. However, the relationship between cellular senescence and clinical outcomes in IPF remains uncertain. Methods: Data from the GSE70867 database were meticulously analyzed in this study. The research employed differential expression analysis, as well as univariate and multivariate Cox regression analysis, to pinpoint senescence-related genes (SRGs) linked to prognosis and construct a prognostic risk model. The model’s clinical relevance and its connection to potential biological processes were systematically assessed in training and testing datasets. Additionally, the expression location of prognosis-related SRGs was identified through immunohistochemical staining, and the correlation between SRGs and immune cell infiltration was deduced using the GSE28221 dataset. Result: The prognostic risk model was constructed based on five SRGs (cellular communication network factor 1, CYR61, stratifin, SFN, megakaryocyte-associated tyrosine kinase, MATK, C-X-C motif chemokine ligand 1, CXCL1, LIM domain, and actin binding 1, LIMA1). Both Kaplan-Meier (KM) curves (p = 0.005) and time-dependent receiver operating characteristic (ROC) analysis affirmed the predictive accuracy of this model in testing datasets, with respective areas under the ROC curve at 1-, 2-, and 3-years being 0.721, 0.802, and 0.739. Furthermore, qRT-RCR analysis and immunohistochemical staining verify the differential expression of SRGs in IPF samples and controls. Moreover, patients in the high-risk group contained higher infiltration levels of neutrophils, eosinophils, and M1 macrophages in BALF, which appeared to be independent indicators of poor prognosis in IPF patients. Conclusion: Our research reveals the effectiveness of the 5 SRGs model in BALF for risk stratification and prognosis prediction in IPF patients, providing new insights into the immune infiltration of IPF progression.
Full article
(This article belongs to the Section Immunology and Immunotherapy)
►
Show Figures
Open AccessArticle
Pigs as Models to Test Cardiovascular Devices
by
Yanina L. Rusakova, Denis S. Grankin, Kseniya S. Podolskaya and Irina Yu. Zhuravleva
Biomedicines 2024, 12(6), 1245; https://doi.org/10.3390/biomedicines12061245 - 3 Jun 2024
Abstract
Pigs as laboratory animals are used in preclinical studies aimed at developing medical devices for cardiac surgery. The anatomy of the cardiovascular system of these animals has been well studied and acknowledged as suitable for use and the testing of new cardiovascular devices
[...] Read more.
Pigs as laboratory animals are used in preclinical studies aimed at developing medical devices for cardiac surgery. The anatomy of the cardiovascular system of these animals has been well studied and acknowledged as suitable for use and the testing of new cardiovascular devices developed for humans. However, there are no morphometric characteristics of the aortic root and thoraco-abdominal part of porcine aorta. This can lead to difficulties in experimental surgery and even result in the death of experimental animals due to the mismatch in the size of the implantable devices. Thus, such information is essential to enhance the efficiency of surgical technologies used for eliminating aortic pathologies in their various sections. The purpose of our research is to study the anatomy of the aorta in mini pigs and to assess whether the size, age, and sex of the animals affect the size of the main structures in their aortas. In addition, we attempted to compare the results obtained by transesophageal echocardiography (TEE) and angiography. We studied 28 laboratory mini pigs, dividing them into three groups by body weight (40–70 kg, 71–90 kg, and 90 kg). We did not find any relationship between the external somatometric characteristics of the animals and the size of their aortas. Animals have individual anatomical variability in their cardiovascular systems, which means that they need to be examined in terms of preoperative planning by any available method—echocardiography, angiography, or multispiral computed tomography (CT).
Full article
(This article belongs to the Special Issue Animal Models for the Study of Cardiovascular Physiology)
►▼
Show Figures
Figure 1
Open AccessArticle
IFN-I Score and Rare Genetic Variants in Children with Systemic Lupus Erythematosus
by
Rinat K. Raupov, Evgeny N. Suspitsin, Elvira M. Kalashnikova, Lubov S. Sorokina, Tatiana E. Burtseva, Vera M. Argunova, Rimma S. Mulkidzhan, Anastasia V. Tumakova and Mikhail M. Kostik
Biomedicines 2024, 12(6), 1244; https://doi.org/10.3390/biomedicines12061244 - 3 Jun 2024
Abstract
Introduction: Interferon I (IFN I) signaling hyperactivation is considered one of the most important pathogenetic mechanisms in systemic lupus erythematosus (SLE). Early manifestation and more severe SLE courses in children suggest a stronger genetic influence in childhood-onset SLE (cSLE). Aim: To evaluate IFN-I
[...] Read more.
Introduction: Interferon I (IFN I) signaling hyperactivation is considered one of the most important pathogenetic mechanisms in systemic lupus erythematosus (SLE). Early manifestation and more severe SLE courses in children suggest a stronger genetic influence in childhood-onset SLE (cSLE). Aim: To evaluate IFN-I score and SLE-associated genetic variants in cSLE. Material and Methods: 80 patients with cSLE were included in the study. IFN I-score was assessed by real-time PCR quantitation of 5 IFN I-regulated transcripts (IFI44L, IFI44, IFIT3, LY6E, MXA1) in 60 patients. Clinical exome sequencing (CES) was performed in 51 patients. Whole-exome sequencing was performed in 32 patients with negative results of CES. Results: 46/60 patients (77%) had elevated IFN-I scores. Leucopenia and skin involvement were associated with over-expression of IFI44 and IFI44L, while hypocomplementemia—with hyperactivation of IFIT3, LY6E, and MX1. No correlation of IFN-I score with disease activity was found. At least one rare genetic variant, potentially associated with SLE, was found in 29 (56.9%) patients. The frequency of any SLE-genetic variants in patients with increased IFN scores was 84%, in patients with normal IFN scores—33%, and in the group whose IFN score was not assessed was 65% (p = 0.040). The majority of genetic variants (74%) are functionally related to nucleic acid sensing and IFN-signaling. The highest frequency of genetic variants was observed in Sakha patients (9/14; 64.3%); three and two unrelated patients had identical variants in PTPN22 and TREX1 genes, respectively. Conclusions: More than half of patients with childhood-onset SLE have rare variants in SLE-associated genes. The IFN-I score could be considered a tool for the selection of patients for further genetic assessment in whom monogenic lupus is suspected.
Full article
(This article belongs to the Special Issue Molecular Mechanisms and Treatment of Rheumatic Diseases)
►▼
Show Figures
Figure 1
Open AccessArticle
Shared Genetic Architectures between Coronary Artery Disease and Type 2 Diabetes Mellitus in East Asian and European Populations
by
Xiaoyi Li, Zechen Zhou, Yujia Ma, Kexin Ding, Han Xiao, Dafang Chen and Na Liu
Biomedicines 2024, 12(6), 1243; https://doi.org/10.3390/biomedicines12061243 - 3 Jun 2024
Abstract
Coronary artery disease (CAD) is a common comorbidity of type 2 diabetes mellitus (T2DM). However, the pathophysiology connecting these two phenotypes remains to be further understood. Combined analysis in multi-ethnic populations can help contribute to deepening our understanding of biological mechanisms caused by
[...] Read more.
Coronary artery disease (CAD) is a common comorbidity of type 2 diabetes mellitus (T2DM). However, the pathophysiology connecting these two phenotypes remains to be further understood. Combined analysis in multi-ethnic populations can help contribute to deepening our understanding of biological mechanisms caused by shared genetic loci. We applied genetic correlation analysis and then performed conditional and joint association analyses in Chinese, Japanese, and European populations to identify the genetic variants jointly associated with CAD and T2DM. Next, the associations between genes and the two traits were also explored. Finally, fine-mapping and functional enrichment analysis were employed to identify the potential causal variants and pathways. Genetic correlation results indicated significant genetic overlap between CAD and T2DM in the three populations. Over 10,000 shared signals were identified, and 587 were shared by East Asian and European populations. Fifty-six novel shared genes were found to have significant effects on both CAD and T2DM. Most loci were fine-mapped to plausible causal variant sets. Several similarities and differences of the involved genes in GO terms and KEGG pathways were revealed across East Asian and European populations. These findings highlight the importance of immunoregulation, neuroregulation, heart development, and the regulation of glucose metabolism in shared etiological mechanisms between CAD and T2DM.
Full article
(This article belongs to the Special Issue Genetics of Chronic Disease)
►▼
Show Figures
Figure 1
Open AccessCase Report
An Unusual Presentation of Synchronous Breast Cancer and Skin Malignancy in a Patient with Lynch Syndrome: A Case Report and Review of the Literature
by
Maiar Elghobashy, Michael Siafakas, Mona Elshafie, Rahul Hejmadi, Naren N. Basu and Abeer M. Shaaban
Biomedicines 2024, 12(6), 1242; https://doi.org/10.3390/biomedicines12061242 - 3 Jun 2024
Abstract
Background: Lynch syndrome is an autosomal dominant condition that leads to an increased risk of many neoplasms. In the United Kingdom, NICE recommends that patients with colorectal and endometrial cancer should be tested for Lynch syndrome. There is conflicting evidence in the literature
[...] Read more.
Background: Lynch syndrome is an autosomal dominant condition that leads to an increased risk of many neoplasms. In the United Kingdom, NICE recommends that patients with colorectal and endometrial cancer should be tested for Lynch syndrome. There is conflicting evidence in the literature on the link between breast cancer and Lynch syndrome. Case presentation: A 54-year-old woman presented with a lump in her right breast with a background of locally advanced colorectal cancer and Lynch syndrome due to a MLH1 gene mutation. A core biopsy showed a grade 3, invasive, triple-negative NST carcinoma. The tumour was triple-negative with patchy positivity for CK14 and CK5/6. Simultaneously, a cystic skin lesion in the contralateral breast was noted, which comprised lesional cells with a proliferation of clear cells and bland basaloid cells. The lesion had evidence of sebaceous differentiation with AR, podoplanin and p63 positivity. MSH1 and PMS2 deficiency was found in the breast and skin lesions. Conclusions: In Lynch syndrome, it is vital to be aware of the increased risk of various types of cancer. This case adds to the body of evidence of the spectrum of malignancies that can be encountered in patients with Lynch syndrome.
Full article
(This article belongs to the Section Cancer Biology and Oncology)
►▼
Show Figures
Figure 1
Open AccessArticle
Prospects for Prostate Cancer Chemotherapy: Cytotoxic Evaluation and Mechanistic Insights of Quinolinequinones with ADME/PK Profile
by
Ayse Tarbin Jannuzzi, Ayse Mine Yilmaz Goler, Abanish Biswas, Subodh Mondal, Vinay N. Basavanakatti, Hatice Yıldırım, Mahmut Yıldız, Nilüfer Bayrak, Venkatesan Jayaprakash and Amaç Fatih TuYuN
Biomedicines 2024, 12(6), 1241; https://doi.org/10.3390/biomedicines12061241 - 3 Jun 2024
Abstract
The evaluation of in vitro biological activity of several previously reported quinolinequinones (AQQ1–5) against 60 human cancer cell lines (NCI-60) used by the National Cancer Institute’s Developmental Therapeutics Program (DTP) contributed to our earlier research on possible anticancer and/or antibacterial agents.
[...] Read more.
The evaluation of in vitro biological activity of several previously reported quinolinequinones (AQQ1–5) against 60 human cancer cell lines (NCI-60) used by the National Cancer Institute’s Developmental Therapeutics Program (DTP) contributed to our earlier research on possible anticancer and/or antibacterial agents. Of interest, NCI-60 screening revealed that two quinolinequinones (AQQ1 and AQQ2) significantly reduced the proliferation of several cancer genotypes. Following the administration of a single dose and five additional doses, all quinolinequinones demonstrated a significant inhibitory effect on the growth of leukemia and other cancer cell lines. Hence, a series of subsequent in vitro biological assessments were performed to further understand the mechanistic impact of the compounds. In MTT assays, it was found that AQQ1 and AQQ2 exhibited higher efficacy against DU-145 cells (IC50 4.18 µM and 4.17 µM, respectively) compared to MDA-MB-231 (IC50 8.27 and 13.33 µM, respectively) and HCT-116 cells (IC50 5.83 and 9.18 µM, respectively). Additionally, AQQ1 demonstrated greater activity in this context. Further investigations revealed that AQQ1 inhibited DU-145 cell growth and migration dose-dependently. Remarkably, arrest of the DU-145 cell cycle at G0/G1 phase and ROS elevation were observed. Pharmacokinetic (PK) studies revealed that AQQ1 has better PK parameters than AQQ2 with %F of 9.83 in rat. Considering the data obtained with human liver microsomal stability studies, AQQ1 should have a better PK profile in human subjects. In silico studies (molecular dynamics) with three kinases (CDK2, CDK4, and MAPK) leading to cell cycle arrest at G0/G1 identified MAPK as a probable target for AQQ1. Taken together, our results showed that AQQ1 could be a potential chemotherapeutic lead molecule for prostate cancer.
Full article
(This article belongs to the Special Issue Medicinal Chemistry in Drug Design and Discovery)
►▼
Show Figures
Figure 1
Open AccessReview
Dendritic Cells: A Bridge between Tolerance Induction and Cancer Development in Transplantation Setting
by
Dario Troise, Barbara Infante, Silvia Mercuri, Valeria Catalano, Elena Ranieri and Giovanni Stallone
Biomedicines 2024, 12(6), 1240; https://doi.org/10.3390/biomedicines12061240 - 3 Jun 2024
Abstract
Dendritic cells (DCs) are a heterogeneous group of antigen-presenting cells crucial for fostering allograft tolerance while simultaneously supporting host defense against infections and cancer. Within the tumor microenvironment, DCs can either mount an immune response against cancer cells or foster immunotolerance, presenting a
[...] Read more.
Dendritic cells (DCs) are a heterogeneous group of antigen-presenting cells crucial for fostering allograft tolerance while simultaneously supporting host defense against infections and cancer. Within the tumor microenvironment, DCs can either mount an immune response against cancer cells or foster immunotolerance, presenting a dual role. In immunocompromised individuals, posttransplant malignancies pose a significant health concern, with DCs serving as vital players in immune responses against cancer cells. Both recipient- and donor-derived DCs play a critical role in the rejection process, infiltrating the transplanted organ and sustaining T-cell responses. The use of immunosuppressive drugs represents the predominant approach to control this immunological barrier in transplanted organs. Evidence has shed light on the immunopharmacology of these drugs and novel strategies for manipulating DCs to promote allograft survival. Therefore, comprehending the mechanisms underlying this intricate microenvironment and the effects of immunosuppressive therapy on DCs is crucial for developing targeted therapies to reduce graft failure rates. This review will delve into the fundamental immunobiology of DCs and provide a detailed exploration of their clinical significance concerning alloimmune responses and posttransplant malignancies.
Full article
(This article belongs to the Special Issue Research of Small-Molecule Therapeutics in Transplantation and Tolerance)
►▼
Show Figures
Figure 1
Open AccessArticle
Investigation of Lung Cancer Cell Response to Cryoablation and Adjunctive Gemcitabine-Based Cryo-Chemotherapy Using the A549 Cell Line
by
Kimberly L. Santucci, Kristi K. Snyder, Robert G. Van Buskirk, John G. Baust and John M. Baust
Biomedicines 2024, 12(6), 1239; https://doi.org/10.3390/biomedicines12061239 - 3 Jun 2024
Abstract
Due to the rising annual incidence of lung cancer (LC), new treatment strategies are needed. While various options exist, many, if not all, remain suboptimal. Several studies have shown cryoablation to be a promising approach. Yet, a lack of basic information pertaining to
[...] Read more.
Due to the rising annual incidence of lung cancer (LC), new treatment strategies are needed. While various options exist, many, if not all, remain suboptimal. Several studies have shown cryoablation to be a promising approach. Yet, a lack of basic information pertaining to LC response to freezing and requirement for percutaneous access has limited clinical use. In this study, we investigated the A549 lung carcinoma cell line response to freezing. The data show that a single 5 min freeze to −15 °C did not affect cell viability, whereas −20 °C and −25 °C result in a significant reduction in viability 1 day post freeze to <10%. These populations, however, were able to recover in culture. Application of a repeat (double) freeze resulted in complete cell death at −25 °C. Studies investigating the impact of adjunctive gemcitabine (75 nM) pretreatment in combination with freezing were then conducted. Exposure to gemcitabine alone resulted in minimal cell death. The combination of gemcitabine pretreatment and a −20 °C single freeze as well as combination treatment with a −15 °C repeat freeze both resulted in complete cell death. This suggests that gemcitabine pretreatment may be synergistically effective when combined with freezing. Studies into the modes of cell death associated with the increased cell death revealed the increased involvement of necroptosis in combination treatment. In summary, these results suggest that repeat freezing to −20 °C to −25 °C results in a high degree of LC destruction. Further, the data suggest that the combination of gemcitabine pretreatment and freezing resulted in a shift of the minimum lethal temperature for LC from −25 °C to −15 °C. These findings, in combination with previous reports, suggest that cryoablation alone or in combination with chemotherapy may provide an improved path for the treatment of LC.
Full article
(This article belongs to the Section Cancer Biology and Oncology)
►▼
Show Figures
Figure 1
Open AccessArticle
AT2R Activation Improves Wound Healing in a Preclinical Mouse Model
by
Julia M. Harrison, Edwin K. Leong, Natasha D. Osborne, Jean S. Marshall and Michael Bezuhly
Biomedicines 2024, 12(6), 1238; https://doi.org/10.3390/biomedicines12061238 - 3 Jun 2024
Abstract
Abnormal skin healing resulting in chronic wounds or hypertrophic scarring remains a major healthcare burden. Here, the antifibrotic angiotensin II type 2 receptor (AT2R) signaling pathway was modulated to determine its impact on cutaneous wound healing. Balb/c mice received two splinted full-thickness wounds.
[...] Read more.
Abnormal skin healing resulting in chronic wounds or hypertrophic scarring remains a major healthcare burden. Here, the antifibrotic angiotensin II type 2 receptor (AT2R) signaling pathway was modulated to determine its impact on cutaneous wound healing. Balb/c mice received two splinted full-thickness wounds. Topical treatments with the selective AT2R agonist compound 21 (C21) and/or selective antagonist PD123319 or saline vehicle were administered until sacrifice on post-wounding days 7 or 10. The rate of wound re-epithelialization was accelerated by PD123319 and combination treatments. In vitro, C21 significantly reduced human fibroblast migration. C21 increased both collagen and vascular densities at days 7 and 10 post-wounding and collagen I:III ratio at day 10, while PD123319 and combination treatments decreased them. Genes associated with regeneration and repair were upregulated by C21, while PD123319 treatment increased the expression of genes associated with inflammation and immune cell chemotaxis. C21 treatment reduced wound total leukocyte and neutrophil staining densities, while PD123319 increased these and macrophage densities. Overall, AT2R activation with C21 yields wounds that mature more quickly with structural, cellular, and gene expression profiles more closely approximating unwounded skin. These findings support AT2R signal modulation as a potential therapeutic target to improve skin quality during wound healing.
Full article
(This article belongs to the Special Issue Skin Fibrosis and Cutaneous Wound Healing)
►▼
Show Figures
Figure 1
Open AccessReview
Combination Therapy for Sustainable Fish Oil Products: Improving Cognitive Function with n-3 PUFA and Natural Ingredients
by
Anthony Arsecularatne, Rotina Kapini, Yang Liu, Dennis Chang, Gerald Münch and Xian Zhou
Biomedicines 2024, 12(6), 1237; https://doi.org/10.3390/biomedicines12061237 - 3 Jun 2024
Abstract
Long-chain polyunsaturated omega-3 fatty acids (n-3 PUFAs), particularly docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), are recommended as beneficial dietary supplements for enhancing cognitive function. Although fish oil (FO) is renowned for its abundant n-3 PUFA content, combining FO with other natural products
[...] Read more.
Long-chain polyunsaturated omega-3 fatty acids (n-3 PUFAs), particularly docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), are recommended as beneficial dietary supplements for enhancing cognitive function. Although fish oil (FO) is renowned for its abundant n-3 PUFA content, combining FO with other natural products is considered as a viable option to support the sustainable development of FO products. This review aims to provide comprehensive insights into the advanced effects of combining FO or its components of DHA and EPA with natural products on protecting cognitive function. In two double-blind random control trials, no advanced effects were observed for adding curcumin to FO on cerebral function protection. However, 16 week’s treatment of FO combined with vitamin E did not yield any advanced effects in cognitive factor scores. Several preclinical studies have demonstrated that combinations of FO with natural products can exhibit advanced effects in addressing pathological components in cognitive impairment, including neuroinflammation, oxidative stress, and neuronal survival. In conclusion, evidence from clinical trials for beneficial use of FO and natural ingredients combination is lacking. Greater cohesion is needed between preclinical and clinical data to substantiate the efficacy of FO and natural product combinations in preventing or slowing the progression of cognitive decline.
Full article
(This article belongs to the Special Issue Pharmacological Targets for Neuroinflammation)
►▼
Show Figures
Figure 1
Open AccessArticle
Ursodeoxycholic Acid Modulates the Interaction of miR-21 and Farnesoid X Receptor and NF-κB Signaling
by
Chi-Yi Peng, Yi-Chun Liao, Yi-Chin Yang, Yi-Wen Hung, Lan-Ru Huang and Yen-Chun Peng
Biomedicines 2024, 12(6), 1236; https://doi.org/10.3390/biomedicines12061236 - 2 Jun 2024
Abstract
(1) Background: This study investigates the effects of Ursodeoxycholic acid (UDCA) on NF-κB signaling, farnesoid X receptor (FXR) singling, and microRNA-21 in HepG2 cells. (2) Methods: HepG2 cells were treated with lipopolysaccharide (LPS) to simulate hepatic inflammation. The investigation focused on the expression
[...] Read more.
(1) Background: This study investigates the effects of Ursodeoxycholic acid (UDCA) on NF-κB signaling, farnesoid X receptor (FXR) singling, and microRNA-21 in HepG2 cells. (2) Methods: HepG2 cells were treated with lipopolysaccharide (LPS) to simulate hepatic inflammation. The investigation focused on the expression of NF-κB activation, which was analyzed using Western blot, confocal microscopy, and Electrophoretic Mobility-shift Assays (EMSA). Additionally, NF-κB and farnesoid X receptor (FXR) singling expressions of micro-RNA-21, COX-2, TNF-α, IL-6, cyp7A1, and shp were assessed by RT-PCR. (3) Results: UDCA effectively downregulated LPS-induced expressions of NF-κB/65, p65 phosphorylation, and also downregulated FXR activity by Western blot. Confocal microscopy and EMSA results confirmed UDCA’s role in modulating NF-κB signaling. UDCA reduced the expressions of LPS-induced COX-2, TNF-α, and IL-6, which were related to NF-κB signaling. UDCA downregulated LPS-induced cyp7A1 gene expression and upregulated shp gene expression, demonstrating selective gene regulation via FXR. UDCA also significantly decreased micro-RNA 21 levels. (4) Conclusions: This study demonstrates UDCA’s potent anti-inflammatory effects on NF-κB and FXR signaling pathways, and thus its potential to modulate hepatic inflammation and carcinogenesis through interactions with NF-κB and FXR. The decrease in micro-RNA 21 expression further underscores its therapeutic potential.
Full article
(This article belongs to the Special Issue Molecular Mechanism in Inflammation and Immunity)
►▼
Show Figures
Figure 1
Open AccessOpinion
Barking Up the Wrong Tree—Motor–Sensory Elements as Prodrome in Autism
by
Meir Lotan
Biomedicines 2024, 12(6), 1235; https://doi.org/10.3390/biomedicines12061235 - 2 Jun 2024
Abstract
Autism spectrum disorder (ASD) has been intensely investigated since the term was first used over 80 years ago. The prevalence of ASD is constantly rising, and, currently, 1:36 children are diagnosed with this disorder. Despite the intense interest in ASD, the origins of
[...] Read more.
Autism spectrum disorder (ASD) has been intensely investigated since the term was first used over 80 years ago. The prevalence of ASD is constantly rising, and, currently, 1:36 children are diagnosed with this disorder. Despite the intense interest in ASD, the origins of this disorder remain obscure. This article explores motor issues and proprioceptive interoception difficulties as the prodrome of ASD. The importance of early intervention in the prognosis of ASD is common knowledge. Yet, since the communicational and social behaviors typical of ASD are observable only after the age of 18 months, diagnosis and early intervention are delayed. Therefore, the quest into the involvement of sensory–motor difficulties as a source of ASD traits, or at least as a potential early indicator, is warranted, with the intention of enabling early diagnosis and early intervention. This article examines the justification for this new avenue of early diagnosis and intervention and may open up a completely different way of viewing ASD. This new point of view may suggest an original path of assessment and intervention in infancy with this group of clients, possibly leading to improved prognosis for children and their families.
Full article
(This article belongs to the Special Issue Diagnostic Biomarkers and Novel Therapeutics Targets for Fragile X Syndrome, Autism Spectrum Disorders and Genetic Neurodevelopmental Diseases: Advances and Challenges)
Open AccessArticle
Hemoglobin and Its Relationship with Fatigue in Long-COVID Patients Three to Six Months after SARS-CoV-2 Infection
by
Somayeh Bazdar, Lizan D. Bloemsma, Nadia Baalbaki, Jelle M. Blankestijn, Merel E. B. Cornelissen, Rosanne J. H. C. G. Beijers, Brigitte M. Sondermeijer, Yolanda van Wijck, George S. Downward and Anke H. Maitland-van der Zee
Biomedicines 2024, 12(6), 1234; https://doi.org/10.3390/biomedicines12061234 - 1 Jun 2024
Abstract
Background: While some long-term effects of COVID-19 are respiratory in nature, a non-respiratory effect gaining attention has been a decline in hemoglobin, potentially mediated by inflammatory processes. In this study, we examined the correlations between hemoglobin levels and inflammatory biomarkers and evaluated the
[...] Read more.
Background: While some long-term effects of COVID-19 are respiratory in nature, a non-respiratory effect gaining attention has been a decline in hemoglobin, potentially mediated by inflammatory processes. In this study, we examined the correlations between hemoglobin levels and inflammatory biomarkers and evaluated the association between hemoglobin and fatigue in a cohort of Long-COVID patients. Methods: This prospective cohort study in the Netherlands evaluated 95 (mostly hospitalized) patients, aged 40–65 years, 3–6 months post SARS-CoV-2 infection, examining their venous hemoglobin concentration, anemia (hemoglobin < 7.5 mmol/L in women and <8.5 mmol/L in men), inflammatory blood biomarkers, average FSS (Fatigue Severity Score), demographics, and clinical features. Follow-up hemoglobin was compared against hemoglobin during acute infection. Spearman correlation was used for assessing the relationship between hemoglobin concentrations and inflammatory biomarkers, and the association between hemoglobin and fatigue was examined using logistic regression. Results: In total, 11 (16.4%) participants were suffering from anemia 3–6 months after SARS-CoV-2 infection. The mean hemoglobin value increased by 0.3 mmol/L 3–6 months after infection compared to the hemoglobin during the acute phase (p-value = 0.003). Whilst logistic regression showed that a 1 mmol/L greater increase in hemoglobin is related to a decrease in experiencing fatigue in Long-COVID patients (adjusted OR 0.38 [95%CI 0.13–1.09]), we observed no correlations between hemoglobin and any of the inflammatory biomarkers examined. Conclusion: Our results indicate that hemoglobin impairment might play a role in developing Long-COVID fatigue. Further investigation is necessary to identify the precise mechanism causing hemoglobin alteration in these patients.
Full article
(This article belongs to the Special Issue Latest Research in Post-COVID (Long COVID): Pathological and Treatment Studies of Sequelae and Complications—2nd Edition)
Open AccessArticle
Perceived Stress and Life Stressors in Adults with and without Fibromyalgia
by
Ha M. Nguyen, Barbara J. Cherry and Laura Zettel-Watson
Biomedicines 2024, 12(6), 1233; https://doi.org/10.3390/biomedicines12061233 - 1 Jun 2024
Abstract
Chronic medical conditions (i.e., chronic widespread pain) may contribute to accelerated/accentuated aging, such that middle-aged individuals with comorbidities may actually show increased declines in physical, cognitive, and mental health compared to normal aging adults. We examined perceived stress, life stressors, and depression in
[...] Read more.
Chronic medical conditions (i.e., chronic widespread pain) may contribute to accelerated/accentuated aging, such that middle-aged individuals with comorbidities may actually show increased declines in physical, cognitive, and mental health compared to normal aging adults. We examined perceived stress, life stressors, and depression in adults with and without fibromyalgia, a chronic pain condition. Ninety-four participants (52% with fibromyalgia, 78% female) aged 50 to 93 were administered the Perceived Stress Scale, Social Readjustment Rating Scale, and Beck Depression Inventory. Hierarchical regression analyses were conducted: the predictor variables were age, gender, fibromyalgia status, depression, and fibromyalgia–depression interaction. The interaction term significantly predicted perceived stress, but not life stressors. Depression significantly predicted stress for Social Readjustment Rating Scale measures after controlling for covariates. Significant associations were found between perceived stress and life stressors in all participants. In addition, those with fibromyalgia were significantly more likely to report higher levels of stress above standardized scores on both the Perceived Stress Scale and the Social Readjustment Rating Scale. Finally, depressive symptoms played a more significant role than fibromyalgia status in predicting life stressors. Conclusions: These findings emphasize the importance of assessing different types of stress and stressors in individuals with chronic widespread pain and/or depression in mid-life and beyond to better treat individuals with these conditions.
Full article
(This article belongs to the Special Issue Molecular Mechanisms of Chronic Pain and New Therapeutic Strategies Volume II)
►▼
Show Figures
Figure 1
Open AccessArticle
Predictive Models for the Transition from Mild Neurocognitive Disorder to Major Neurocognitive Disorder: Insights from Clinical, Demographic, and Neuropsychological Data
by
Anna Tsiakiri, Christos Bakirtzis, Spyridon Plakias, Pinelopi Vlotinou, Konstantinos Vadikolias, Aikaterini Terzoudi and Foteini Christidi
Biomedicines 2024, 12(6), 1232; https://doi.org/10.3390/biomedicines12061232 - 1 Jun 2024
Abstract
Neurocognitive disorders (NCDs) are progressive conditions that severely impact cognitive function and daily living. Understanding the transition from mild to major NCD is crucial for personalized early intervention and effective management. Predictive models incorporating demographic variables, clinical data, and scores on neuropsychological and
[...] Read more.
Neurocognitive disorders (NCDs) are progressive conditions that severely impact cognitive function and daily living. Understanding the transition from mild to major NCD is crucial for personalized early intervention and effective management. Predictive models incorporating demographic variables, clinical data, and scores on neuropsychological and emotional tests can significantly enhance early detection and intervention strategies in primary healthcare settings. We aimed to develop and validate predictive models for the progression from mild NCD to major NCD using demographic, clinical, and neuropsychological data from 132 participants over a two-year period. Generalized Estimating Equations were employed for data analysis. Our final model achieved an accuracy of 83.7%. A higher body mass index and alcohol drinking increased the risk of progression from mild NCD to major NCD, while female sex, higher praxis abilities, and a higher score on the Geriatric Depression Scale reduced the risk. Here, we show that integrating multiple factors—ones that can be easily examined in clinical settings—into predictive models can improve early diagnosis of major NCD. This approach could facilitate timely interventions, potentially mitigating the progression of cognitive decline and improving patient outcomes in primary healthcare settings. Further research should focus on validating these models across diverse populations and exploring their implementation in various clinical contexts.
Full article
(This article belongs to the Special Issue Crosstalk between Depression, Anxiety, Dementia, and Chronic Pain: Comorbidity in Behavioral Neurology and Neuropsychiatry Volume III)
►▼
Show Figures
Figure 1
Open AccessArticle
A 5-Year Follow-Up after Endovascular Treatment of 402 Intracranial Aneurysms—A Single-Centre Experience
by
Ana Repić Buličić, David Ozretić, Marko Radoš, Josip Ljevak, Antonela Bazina Martinović and Zdravka Poljaković Skurić
Biomedicines 2024, 12(6), 1231; https://doi.org/10.3390/biomedicines12061231 - 1 Jun 2024
Abstract
The aim of our study was to evaluate the early and long-term clinical and morphological outcomes of the endovascular treatment of ruptured and non-ruptured intracranial aneurysms in a cohort of patients from a single centre. We retrospectively analysed the treatment outcomes of 402
[...] Read more.
The aim of our study was to evaluate the early and long-term clinical and morphological outcomes of the endovascular treatment of ruptured and non-ruptured intracranial aneurysms in a cohort of patients from a single centre. We retrospectively analysed the treatment outcomes of 402 endovascularly treated intracranial aneurysms with an average follow-up of 5.5 years. All included patients were treated with endovascular techniques (coil, stent or both). We analysed patient demographics, risk factors for an aneurysm rupture, aneurysm characteristics, and clinical and angiographic complications and outcomes. We analysed and compared the data from the two groups, ruptured aneurysms (RAs) and unruptured aneurysms (UAs), separately. Out of the 318 patients included, a good early clinical outcome was achieved in 78.5% of RAs and in 95.3% of UAs. No complications occurred in 87.71% of patients with UAs and in 80.45% with RAs. The periprocedural rupture rate for UAs and RAs was 0.8% and 2.2%, respectively. The rate of thromboembolic events was 4.8 and 8% for UAs and RAs, respectively. A retreatment due to the recanalisation was required in 9.21% of patients with UAs and in 16.66% of patients with RAs. The results from our centre showed an overall favourable clinical outcome with acceptable periprocedural complications for both RAs and UR aneurysms and proved the endovascular method as safe and effective in the treatment of intracranial aneurysms.
Full article
(This article belongs to the Section Molecular and Translational Medicine)
►▼
Show Figures
Figure 1
Open AccessReview
Microbubble-Enhanced Focused Ultrasound for Infiltrating Gliomas
by
Alexandra A. Seas, Adarsha P. Malla, Nima Sharifai, Jeffrey A. Winkles, Graeme F. Woodworth and Pavlos Anastasiadis
Biomedicines 2024, 12(6), 1230; https://doi.org/10.3390/biomedicines12061230 - 1 Jun 2024
Abstract
Infiltrating gliomas are challenging to treat, as the blood-brain barrier significantly impedes the success of therapeutic interventions. While some clinical trials for high-grade gliomas have shown promise, patient outcomes remain poor. Microbubble-enhanced focused ultrasound (MB-FUS) is a rapidly evolving technology with demonstrated safety
[...] Read more.
Infiltrating gliomas are challenging to treat, as the blood-brain barrier significantly impedes the success of therapeutic interventions. While some clinical trials for high-grade gliomas have shown promise, patient outcomes remain poor. Microbubble-enhanced focused ultrasound (MB-FUS) is a rapidly evolving technology with demonstrated safety and efficacy in opening the blood-brain barrier across various disease models, including infiltrating gliomas. Initially recognized for its role in augmenting drug delivery, the potential of MB-FUS to augment liquid biopsy and immunotherapy is gaining research momentum. In this review, we will highlight recent advancements in preclinical and clinical studies that utilize focused ultrasound to treat gliomas and discuss the potential future uses of image-guided precision therapy using focused ultrasound.
Full article
(This article belongs to the Special Issue Gliomas: Signaling Pathways, Molecular Mechanisms and Novel Therapies)
►▼
Show Figures
Figure 1
Open AccessReview
The Role of Lipoprotein(a) in Peripheral Artery Disease
by
Nicholas Pavlatos and Dinesh K. Kalra
Biomedicines 2024, 12(6), 1229; https://doi.org/10.3390/biomedicines12061229 - 1 Jun 2024
Abstract
Lipoprotein(a) is a low-density-lipoprotein-like particle that consists of apolipoprotein(a) bound to apolipoprotein(b). It has emerged as an established causal risk factor for atherosclerotic cardiovascular disease, stroke, and aortic valve stenosis through multifactorial pathogenic mechanisms that include inflammation, atherogenesis, and thrombosis. Despite an estimated
[...] Read more.
Lipoprotein(a) is a low-density-lipoprotein-like particle that consists of apolipoprotein(a) bound to apolipoprotein(b). It has emerged as an established causal risk factor for atherosclerotic cardiovascular disease, stroke, and aortic valve stenosis through multifactorial pathogenic mechanisms that include inflammation, atherogenesis, and thrombosis. Despite an estimated 20% of the global population having elevated lipoprotein(a) levels, testing remains underutilized due to poor awareness and a historical lack of effective and safe therapies. Although lipoprotein(a) has a strong association with coronary artery disease and cerebrovascular disease, its relationship with peripheral artery disease is less well established. In this article, we review the epidemiology, biology, and pathogenesis of lipoprotein(a) as it relates to peripheral artery disease. We also discuss emerging treatment options to help mitigate major adverse cardiac and limb events in this population.
Full article
(This article belongs to the Special Issue Cardiovascular and Metabolic Disease: New Treatment and Future Directions—the 3rd Edition)
Open AccessArticle
Impact of TNFRSF1B (rs3397, rs1061624 and rs1061622) and IL6 (rs1800796, rs1800797 and rs1554606) Gene Polymorphisms on Inflammatory Response in Patients with End-Stage Kidney Disease Undergoing Dialysis
by
Susana Coimbra, Susana Rocha, Cristina Catarino, Maria João Valente, Petronila Rocha-Pereira, Maria Sameiro-Faria, José Gerardo Oliveira, José Madureira, João Carlos Fernandes, Vasco Miranda, Luís Belo, Elsa Bronze-da-Rocha and Alice Santos-Silva
Biomedicines 2024, 12(6), 1228; https://doi.org/10.3390/biomedicines12061228 - 31 May 2024
Abstract
We aimed to study the impact of polymorphisms in the genes encoding interleukin-6 (IL6) and tumor necrosis factor receptor-2 (TNFR2), reported to be mortality risk predictors, in patients with end-stage kidney disease (ESKD) undergoing dialysis. TNFRSF1B (rs3397, rs1061624, and rs1061622) and IL6 (rs1800796,
[...] Read more.
We aimed to study the impact of polymorphisms in the genes encoding interleukin-6 (IL6) and tumor necrosis factor receptor-2 (TNFR2), reported to be mortality risk predictors, in patients with end-stage kidney disease (ESKD) undergoing dialysis. TNFRSF1B (rs3397, rs1061624, and rs1061622) and IL6 (rs1800796, rs1800797, and rs1554606) polymorphisms were studied in patients with ESKD and controls; the genotype and allele frequencies and the associations with inflammatory and erythropoiesis markers were determined; deaths were recorded throughout the following two years. The genotype and allele frequencies for the TNFRSF1B rs3397 polymorphism were different in these patients compared to those in the controls and the global and European populations, and patients with the C allele were less common. Patients with the CC genotype for TNFRSF1B rs3397 presented higher hemoglobin and erythrocyte counts and lower TNF-α levels, suggesting a more favorable inflammatory response that seems to be associated with erythropoiesis improvement. Patients with the GG genotype for TNFRSF1B rs1061622 showed lower serum ferritin levels. None of the TNFRSF1B (rs3397, rs1061624, and rs1061622) or IL6 (rs1800796, rs1800797, and rs1554606) polymorphisms had a significant impact on the all-cause mortality rate of Portuguese patients with ESKD.
Full article
(This article belongs to the Special Issue New Advances in Chronic Kidney Disease: Biology, Diagnosis and Therapy)
Open AccessArticle
Association of Circulating Markers of Microbial Translocation and Hepatic Inflammation with Liver Injury in Patients with Type 2 Diabetes
by
Leila Gobejishvili, Vatsalya Vatsalya, Diana V. Avila, Yana B. Feygin, Craig J. McClain, Sriprakash Mokshagundam and Shirish Barve
Biomedicines 2024, 12(6), 1227; https://doi.org/10.3390/biomedicines12061227 - 31 May 2024
Abstract
Background: Virtually the entire spectrum of liver disease is observed in association with type 2 diabetes mellitus (T2DM); indeed, T2DM is now the most common cause of liver disease in the U.S. We conducted a pilot study to investigate the relevance of increased
[...] Read more.
Background: Virtually the entire spectrum of liver disease is observed in association with type 2 diabetes mellitus (T2DM); indeed, T2DM is now the most common cause of liver disease in the U.S. We conducted a pilot study to investigate the relevance of increased microbial translocation and systemic inflammation in the development of liver injury in patients with T2DM. Methods: Patients with T2DM (n = 17) and non-diabetic controls (NDC; n = 11) aged 25–80 yrs. participated in this study. Serum levels of endotoxin, calprotectin, soluble CD14 and CD163, and several inflammatory cytokines were measured. In addition to standard liver injury markers, ALT and AST, novel serum markers of liver injury, keratin 18 (K-18) M30 (apoptosis-associated caspase-cleaved keratin 18), and M65 (soluble keratin 18) were evaluated. Statistical analyses were performed using the Mann–Whitney test to assess differences between study groups. Pearson’s correlation analysis was performed to determine the strength of association between two variables using GraphPad Prism 9.5.0 software. Results: Patients with T2DM had significantly higher levels of sCD14 in comparison to NDC, suggesting an increase in gut permeability, microbial translocation, and monocyte/macrophage activation. Importantly, relevant to the ensuing inflammatory responses, the increase in sCD14 in patients with T2DM was accompanied by a significant increase in sCD163, a marker of hepatic Kupffer cell activation and inflammation. Further, a positive correlation was observed between sCD163 and endotoxin and sCD14 in T2DM patients but not in NDC. In association with these changes, keratin 18 (K-18)-based serum markers (M65 and M30) that reflect hepatocyte death were significantly higher in the T2DM group indicating ongoing liver injury. Notably, both M65 and M30 levels correlated with sCD14 and sCD163, suggesting that immune cell activation and hepatic inflammation may be linked to the development of liver injury in T2DM. Conclusions: These findings suggest that the pathogenic changes in the gut–liver axis, marked by increased microbial translocation, may be a major component in the etiology of hepatocyte inflammation and injury in patients with T2DM. However, larger longitudinal studies, including histological evidence, are needed to confirm these observations.
Full article
(This article belongs to the Special Issue Advanced Research in Metabolic Syndrome)
Journal Menu
► ▼ Journal Menu-
- Biomedicines Home
- Aims & Scope
- Editorial Board
- Reviewer Board
- Topical Advisory Panel
- Instructions for Authors
- Special Issues
- Topics
- Sections & Collections
- Article Processing Charge
- Indexing & Archiving
- Editor’s Choice Articles
- Most Cited & Viewed
- Journal Statistics
- Journal History
- Journal Awards
- Society Collaborations
- Conferences
- Editorial Office
Journal Browser
► ▼ Journal BrowserHighly Accessed Articles
Latest Books
E-Mail Alert
News
Topics
Topic in
Biomedicines, Cancers, JFB, Nanomaterials, Polymers
Advanced Functional Materials for Regenerative Medicine
Topic Editors: Antonino Morabito, Luca ValentiniDeadline: 6 June 2024
Topic in
Biomedicines, Current Oncology, Diagnostics, Gastrointestinal Disorders, JCM
Advances in Gastrointestinal and Liver Disease: From Physiological Mechanisms to Clinical Practice
Topic Editors: Davide Giuseppe Ribaldone, Gian Paolo CavigliaDeadline: 20 June 2024
Topic in
BioChem, Biomedicines, Biomolecules, IJMS, Metabolites, Molecules
Natural Products in Prevention and Therapy of Metabolic Syndrome
Topic Editors: Jianbo Wan, Ligen LinDeadline: 30 June 2024
Topic in
Cancers, Diagnostics, JCM, Current Oncology, Gastrointestinal Disorders, Biomedicines
Hepatobiliary and Pancreatic Diseases: Novel Strategies of Diagnosis and Treatments
Topic Editors: Alessandro Coppola, Damiano Caputo, Roberta Angelico, Domenech Asbun, Chiara MazzarelliDeadline: 20 July 2024
Conferences
Special Issues
Special Issue in
Biomedicines
Drugs Targeting the Disease Progression, Cognitive Impairment, Anxiety and Other Co-morbidities in Epilepsy: From Bench to Bedside
Guest Editors: Diana Cunha-Reis, Paulo Correia-de-SáDeadline: 15 June 2024
Special Issue in
Biomedicines
Advanced Research in Tissue Engineering and Cellular Culture and Their Applications
Guest Editors: Victor Palarie, Peer Wolfgang KämmererDeadline: 30 June 2024
Special Issue in
Biomedicines
Recent Updates on Adrenal Tumors
Guest Editors: Piotr Glinicki, Alicja SzatkoDeadline: 15 July 2024
Special Issue in
Biomedicines
State-of-the-Art and Novel Approaches in Molecular and Translational Medicine in Europe
Guest Editor: Vasileios TzounakasDeadline: 31 July 2024
Topical Collections
Topical Collection in
Biomedicines
OMICs and Complex Diseases
Collection Editors: Mostafa Dianatinasab, Anke Wesselius, Amin Salehi-Abargouei
Topical Collection in
Biomedicines
Feature Papers in Cancer Biology and Therapeutics
Collection Editor: Veronique Baud
Topical Collection in
Biomedicines
Feature Papers in Gene and Cell Therapy
Collection Editor: Bernard Lebleu
Topical Collection in
Biomedicines
Feature Papers in Microbiology in Human Health and Disease
Collection Editor: Ryota Niikura