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        <title>Experimental Biology and Medicine | Anatomy/Pathology section | New and Recent Articles</title>
        <link>https://www.ebm-journal.org/journals/experimental-biology-and-medicine/sections/anatomypathology</link>
        <description>RSS Feed for Anatomy/Pathology section in the Experimental Biology and Medicine journal | New and Recent Articles</description>
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        <pubDate>2026-04-10T13:06:22.823+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10746</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10746</link>
        <title><![CDATA[Platelet-rich plasma in peripheral nerve injury repair: a comprehensive review of mechanisms, clinical applications, and therapeutic potential]]></title>
        <pubdate>2025-09-23T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Kai Shang</author><author>Yang Liu</author><author>Abdul Qadeer</author>
        <description><![CDATA[Peripheral nerve injuries (PNIs) pose a significant clinical challenge, often leading to incomplete functional recovery despite current treatments. Platelet-rich plasma (PRP), which contains high levels of growth factors and bioactive molecules, has emerged as a promising regenerative therapy for nerve repair and restoring function. This review consolidates current evidence on PRP applications in treating peripheral nerve injuries, examining molecular mechanisms, clinical outcomes, and therapeutic potential. PRP markedly enhances nerve regeneration, improves recovery of sensory and motor functions, and alleviates neuropathic pain across various nerve injuries. It promotes axonal growth, reduces scar formation, stimulates Schwann cell proliferation, and modulates inflammation through the release of neurotrophic factors, including PDGF, VEGF, TGF-β, and IGF-1. Combining PRP with surgical techniques and biomaterial scaffolds yields better therapeutic results. Key factors influencing efficacy include platelet concentration, leukocyte content, activation methods, and patient-specific variables. PRP is a safe and effective option for peripheral nerve injury repair. However, challenges persist in standardizing preparation protocols, optimizing treatment timing, and fully understanding molecular mechanisms. Future research should focus on personalized PRP formulations, combination therapies, and large-scale randomized controlled trials to develop definitive clinical guidelines.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10607</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10607</link>
        <title><![CDATA[Assessing the developmental effects of fentanyl and impacts on lipidomic profiling using neural stem cell models]]></title>
        <pubdate>2025-06-25T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Cheng Wang</author><author>Jinchun Sun</author><author>Rohini Donakonda</author><author>Richard Beger</author><author>Leah E. Latham</author><author>Leihong Wu</author><author>Shuliang Liu</author><author>Joseph P. Hanig</author><author>Fang Liu</author>
        <description><![CDATA[Fentanyl is a potent and short-acting opioid that is often given to pediatric patients during surgery to relieve pain and as an adjunct to anesthesia. Its effects on the developing brain are yet to be determined. In the present study, commercially available human neural stem cells (NSCs) were used to model the effects of fentanyl on the developing human brain. We determined the dose dependent effects and temporal relationships between fentanyl exposures and NSC health, viability, and differentiation. Markers of mitochondrial health [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetra-zolium bromide (MTT)] and cell death/damage [lactate dehydrogenase (LDH)] were monitored to determine the dose response effects of fentanyl on NSC viability. In addition, lipidomics analysis was conducted to investigate lipid profile changes in differentiated neural cells treated with fentanyl. Fentanyl did not cause a significant increase in LDH release, nor MTT reduction after 24-h exposure at concentrations of 0.5, 1.0, 3.0, 10, or 100 μM, for both NSCs and differentiated neural cells. Lipidomics data showed the top 15 most variable important in projection (VIP) lipid species (the higher the VIP scores, the bigger changes in treated groups vs. controls), including lysophosphatidylcholines (LPCs), lysophosphatidylethanolamines (LPEs), ceramides (CER), cholesterol esters (ChEs) and sphingosine (SPH). The lipidomic data indicate that LPC (16:0), LPC (16:1), LPC (18:1), CER (d18:0_22:0), CER (d18:2_18:0), CER(d18:2_24:1) were significantly increased, and only ChE (24:5) and SPH (d18:1) were significantly decreased in the highest dose group versus control. These data indicated that fentanyl exposure (24-h) did not induce detectable cell death. However, a lipidomic analysis indicated that fentanyl may affect immature neural cell functions through modifying lipid composition and lipid metabolism. These data indicated that despite the absence of clear neurodegeneration, fentanyl may still have a negative impact on the developing brain.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10608</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10608</link>
        <title><![CDATA[The effects of cannabidiol and its main metabolites on human neural stem cells]]></title>
        <pubdate>2025-06-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Leah E. Latham</author><author>Qiang Gu</author><author>Shuliang Liu</author><author>Cheng Wang</author><author>Fang Liu</author>
        <description><![CDATA[Cannabidiol (CBD) has been used for different purposes by different populations in recent years. When consumed by pregnant women, CBD can pass through the placenta and enter the fetal blood stream. There is concern over adverse effects of fetal exposure to CBD and its major metabolites (7-OH-CBD and 7-COOH-CBD). In the present study, human neural stem cells (NSCs) were treated with CBD and its metabolites at different concentrations for various durations to understand how the drug may affect fetal brain development. NSCs were also treated with delta-9 tetrahydrocannabinol (THC) for comparison purposes. CBD, 7-OH-CBD and 7-COOH-CBD dose-dependently reduced NSC viability. CBD and 7-OH-CBD reduced NSC number at the G1 phase. A 24 h exposure did not cause significant change in NSC proliferation. At concentrations comparable to those detected in human blood, longer exposures to CBD, 7-OH-CBD and 7-COOH-CBD caused more obvious cell death. After NSCs differentiation, CBD treatment reduced GFAP and cannabinoid receptor 2 (CB2) expression. THC treatment reduced the GFAP expression, but the change in CB2 expression did not reach statistical significance. The expression of cannabinoid receptor 1 (CB1) and beta-tubulin III were not significantly altered by drug exposures. The study demonstrated that clinically relevant concentrations of CBD, 7-OH-CBD and 7-COOH-CBD affect basic physiological features of human NSCs. After NSC differentiation, the reduced expression of CB2 receptors and GFAP on differentiated cells further indicated the vulnerability of developing central nervous system to CBD and THC. These data will help to contextualize in vivo neurodevelopmental studies that may not accurately model human metabolite profiles of CBD.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10606</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10606</link>
        <title><![CDATA[Assessing potential desflurane-induced neurotoxicity using nonhuman primate neural stem cell models]]></title>
        <pubdate>2025-06-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Cheng Wang</author><author>Leah E. Latham</author><author>Shuliang Liu</author><author>John Talpos</author><author>Tucker A. Patterson</author><author>Joseph P. Hanig</author><author>Fang Liu</author>
        <description><![CDATA[Safety concerns about general anesthetics (GA), such as desflurane (a commonly used gaseous anesthetic agent), arose from studies documenting neural cell death and behavioral changes after early-life exposure to anesthetics and compounds with related modes of action. Neural stem cells (NSCs) can recapitulate most critical events during central nervous system (CNS) development in vivo and, therefore, represent a valuable in vitro model for evaluating potential desflurane-induced developmental neurotoxicity. In this study, NSCs harvested from the hippocampus of a gestational day 80 monkey brain were applied to explore the temporal relationships between desflurane exposures and neural stem cell health, proliferation, differentiation, and viability. At clinically relevant doses (5.7%), desflurane exposure did not result in significant changes in NSC viability [lactate dehydrogenase (LDH) release] and NSC proliferation profile/rate by Cell Cycle Assay, in both short term (3 h) and prolonged (24 h) exposure groups. However, when monkey NSCs were guided to differentiate into neural cells (including neurons, astrocytes, and oligodendrocytes), and then exposed to desflurane (5.7%), no significant changes were detected in LDH release after a 3-h exposure, but a significant elevation in LDH release into the culture medium was observed after a 24-h exposure. Desflurane (24 h)-induced neural damage was further supported by increased expression levels of multiple cytokines, e.g., G-CSF, IL-12, IL-9, IL-10, and TNF-α compared with the controls. Additionally, our immunocytochemistry and flow cytometry data demonstrated a remarkable attenuation of differentiated neurons as evidenced by significantly decreased numbers of polysialic acid neural cell adhesion molecule (PSA-NCAM)-positive cells in the desflurane-exposed (prolonged) cultures. Our data suggests that at the clinically relevant concentration, desflurane did not induce NSC damage/death, but impaired the differentiated neuronal cells after prolonged exposure. Collectively, PSA-NCAM could be essential for neuronal viability. Desflurane-induced neurotoxicity was primarily associated with the loss of differentiated neurons. Changes in the neuronal specific marker, PSA-NCAM, may help understand the underlying mechanisms associated with anesthetic-induced neuronal damage. These findings should be helpful/useful for the understanding of the diverse effects of desflurane exposure on the developing brain and could be used to optimize the usage of these agents in the pediatric setting.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10066</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10066</link>
        <title><![CDATA[Impaired fracture healing is associated with callus chondro-osseous junction abnormalities in periostin-null and osteopontin-null mice]]></title>
        <pubdate>2025-01-22T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Marc Teitelbaum</author><author>Maya D. Culbertson</author><author>Charlene Wetterstrand</author><author>J. Patrick O’Connor</author>
        <description><![CDATA[Periostin and osteopontin are matricellular proteins abundantly expressed in bone fracture callus. Null mutation of either the periostin (Postn) gene or the osteopontin (Spp1) gene can impair bone fracture healing. However, the cell and molecular pathways affected by loss of POSTN or SPP1 which lead to impaired fracture healing are not well understood. To identify potential pathways, a detailed radiological, histological, and immunohistochemical analysis of femur fracture healing in Postn-null (PostnKO), Spp1-null (Spp1KO), and normal (WT) mice was performed. Apparent changes in specific protein levels identified by immunohistochemistry were confirmed by mRNA quantitation. Comparisons between the PostnKO and Spp1KO fracture calluses were confounded by interactions between the two genes; loss of Postn reduced Spp1 expression and loss of Spp1 reduced Postn expression. Consequently, alterations in fracture healing between mice heterozygous for the Postn-null allele (PostnHET) as well as the PostnKO and Spp1KO mice were similar. Calluses from PostnHET, PostnKO, and Spp1KO mice all had dysmorphic chondro-osseous junctions and reduced numbers of osteoclasts. The dysmorphic chondro-osseous junctions in the PostnHET, PostnKO, and Spp1KO calluses were associated with reduced numbers of MMP-13 expressing hypertrophic chondrocytes, consistent with delayed cartilage resolution. Unlike collagen X expressing callus chondrocytes, chondrocytes only expressed MMP-13 when localized to the chondro-osseous junction or after traversing the chondro-osseous junction. Cyclooxygenase-2 (COX-2) expression also appeared to be reduced in osteoclasts from the PostnHET, PostnKO, and Spp1KO calluses, including in those osteoclasts localized at the chondro-osseous junction. The results indicate that POSTN and SPP1 are necessary for normal chondro-osseous junction formation and that signaling from the chondro-osseous junction, possibly from COX-2 expressing osteoclasts, regulates callus vasculogenesis and chondrocyte hypertrophy necessary for endochondral ossification during fracture healing.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10185</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10185</link>
        <title><![CDATA[Reversal of atherosclerosis by restoration of vascular copper homeostasis]]></title>
        <pubdate>2024-06-24T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Xiao Zuo</author><author>Xueqin Ding</author><author>Yaya Zhang</author><author>Y. James Kang</author>
        <description><![CDATA[Atherosclerosis has traditionally been considered as a disorder characterized by the accumulation of cholesterol and thrombotic materials within the arterial wall. However, it is now understood to be a complex inflammatory disease involving multiple factors. Central to the pathogenesis of atherosclerosis are the interactions among monocytes, macrophages, and neutrophils, which play pivotal roles in the initiation, progression, and destabilization of atherosclerotic lesions. Recent advances in our understanding of atherosclerosis pathogenesis, coupled with results obtained from experimental interventions, lead us to propose the hypothesis that atherosclerosis may be reversible. This paper outlines the evolution of this hypothesis and presents corroborating evidence that supports the potential for atherosclerosis regression through the restoration of vascular copper homeostasis. We posit that these insights may pave the way for innovative therapeutic approaches aimed at the reversal of atherosclerosis.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10175</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10175</link>
        <title><![CDATA[Topical naltrexone increases aquaporin 5 production in the lacrimal gland and restores tear production in diabetic rats]]></title>
        <pubdate>2024-05-02T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>David Diaz</author><author>Joseph P. Sassani</author><author>Ian S. Zagon</author><author>Patricia J. McLaughlin</author>
        <description><![CDATA[Diabetes mellitus is a prevalent disease that is often accompanied by ocular surface abnormalities including delayed epithelial wound healing and decreased corneal sensitivity. The impact of diabetes on the lacrimal functional unit (LFU) and the structures responsible for maintaining tear homeostasis, is not completely known. It has been shown that the Opioid Growth Factor Receptor (OGFr), and its ligand, Opioid Growth Factor (OGF), is dysregulated in the ocular surface of diabetic rats leading to overproduction of the inhibitory growth peptide OGF. The opioid antagonist naltrexone hydrochloride (NTX) blocks the OGF-OGFr pathway, and complete blockade following systemic or topical treatment with NTX restores the rate of re-epithelialization of corneal epithelial wounds, normalizes corneal sensitivity, and reverses dry eye in diabetic animal models. These effects occur rapidly and within days of initiating treatment. The present study was designed to understand mechanisms related to the fast reversal (<5 days) of dry eye by NTX in type 1 diabetes (T1D) by investigating dysregulation of the LFU. The approach involved examination of the morphology of the LFU before and after NTX treatment. Male and female adult Sprague-Dawley rats were rendered hyperglycemic with streptozotocin, and after 6 weeks rats were considered to be a T1D model. Rats received topical NTX twice daily to one eye for 10 days. During the period of treatment, tear production and corneal sensitivity were recorded. On day 11, animals were euthanized and orbital tissues including conjunctiva, eyelids, and lacrimal glands, were removed and processed for histologic examination including immunohistochemistry. Male and female T1D rats had significantly decreased tear production and corneal insensitivity, significantly decreased number and size of lacrimal gland acini, decreased expression of aquaporin-5 (AQP5) protein and decreased goblet cell size. Thus, 10 days of NTX treatment restored tear production and corneal sensitivity to normal values, increased AQP5 expression, and restored the surface area of goblet cells to normal. NTX had no effect on the number of lacrimal gland acini or the number of conjunctival goblet cells. In summary, blockade of the OGF-OGFr pathway with NTX reversed corneal and lacrimal gland complications and restored some components of tear homeostasis confirming the efficacy of topical NTX as a treatment for ocular defects in diabetes.]]></description>
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