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Tabata, Y.

Publications and source records attributed to Tabata, Y..

6 recordsLinked to original sources

A Novel Metric for Quantifying the Sustainability of Phage-Mediated Bacterial Suppression

The global spread of antimicrobial-resistant (AMR) bacteria represents one of the greatest threats to modern medicine, making the development of novel therapeutic strategies increasingly urgent. Phage therapy, which exploits bacteriophages (phages, viruses that specifically infect and kill bacteria) has regained attention as a therapeutic approach for multidrug-resistant infections. One critical determinant of treatment outcome is the capacity of phages to sustain bacterial growth suppression; however, no metric has previously existed to directly quantify the duration of effective lytic activity. Here, we propose the Sustainability Index (SusI), a novel metric that quantifies both the duration and extent of phage-mediated bacterial growth suppression, which is restricted to the primary lysis period from lysis initiation to resistance emergence. Evaluation of individual phages and two-phage cocktails against both laboratory and clinical isolates of Escherichia coli demonstrated that SusI provides information independent of the Virulence Index, which primarily reflects bactericidal activity during the initial phase of infection, and serves as a complementary metric to the Suppression Index, which may incorporate behavior beyond primary lysis. Cocktails composed of phages targeting different receptors specificities consistently exhibited higher SusI values, consistent with the notion that multifaceted selective pressure delays resistance emergence. Furthermore, in a mouse model of systemic infection established by intraperitoneal administration, cocktails with higher SusI values demonstrated superior therapeutic efficacy. These results confirm SusI as a practical metric for rational phage cocktail design. As phage therapy advances toward clinical implementation, standardized quantitative metrics such as SusI are expected to facilitate evidence-based selection of therapeutic phages across diverse pathogens and infection conditions. ImportanceThe global spread of antimicrobial-resistant bacteria is making bacterial infections increasingly difficult to treat. Phage therapy, which uses bacteriophages (viruses that specifically infect bacteria), has re-emerged as a therapeutic alternative; however, reliable methods to determine in advance which phages will be therapeutically effective remain limited. Current evaluation metrics are well-suited for quantifying how rapidly phages kill bacteria but were not designed to directly measure how long lytic activity is sustained before resistant bacteria emerge. Here, we developed the Sustainability Index (SusI), a novel metric that specifically quantifies the duration of effective bacterial growth suppression. Evaluation of multiple phages and their combinations (cocktails) against both laboratory and clinical bacterial isolates demonstrated that SusI can distinguish phage combinations that existing metrics fail to differentiate. Moreover, in a mouse model of lethal bacterial infection, higher SusI values correlated with improved therapeutic outcomes. SusI has potential as a practical tool for selecting phages with greater likelihood of therapeutic success.

microbiology↗

Mesenchymal Stem Cell Membrane Coating of Gelatin Nanospheres with Drug Release Ability for Inflammatory Tissue Targeting

Improvements in drug delivery have been achieved using nanospheres to prolong drug efficacy, accelerate absorption, and target tissues with ongoing inflammation. Although nanospheres have numerous pharmacokinetic advantages their tissue-targeting ability is poor. In contrast, mesenchymal stem cells (MSC) accumulate in high numbers in inflammatory tissues via the interaction between CXC-chemokine receptor 4 (CXCR4) expressed on MSC and stromal cell-derived factor 1 (SDF-1) secreted during inflammation. Therefore, this study investigated coating gelatin nanospheres (GNS) with MSC membranes (MSC-GNS) by extrusion and ultrasonication methods to enhance their inflammatory tissue tropism. {zeta}-potential measurements, western blotting and single-particle analysis of MSC-GNS by flow cytometry demonstrated the GNS surface was successfully coated with MSC membranes. Dot blotting demonstrated the binding ability of CXCR4 for SDF-1 was retained by MSC-GNS but absent for MSC-membrane-free GNS. The blood clearance of MSC-GNS was examined by their intravenous injection into mice. Although MSC-GNS and GNS were retained during the early distribution phase, MSC-GNS had a higher retention than GNS during the later elimination phase. Finally, we investigated the tissue distribution of MSC-GNS by intravenous injection into a mouse model of liver fibrosis and their potential therapeutic effect on liver fibrosis. We found a higher accumulation of MSC-GNS in inflamed livers and higher blood retention compared with MSC-membrane-free GNS. Furthermore, MSC-GNS loaded with an anti-fibrotic agent (LSKL, a 4-amino acid peptide that inhibits fibrosis progression) had an enhanced therapeutic effect on liver fibrosis than uncoated nanoparticles. Therefore, MSC-GNS might be a drug carrier with inflammatory tissue targeting and controlled drug release abilities. Synopsis Table of Contents Graphic O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=81 SRC="FIGDIR/small/657318v1_ufig1.gif" ALT="Figure 1"> View larger version (22K): org.highwire.dtl.DTLVardef@12331d8org.highwire.dtl.DTLVardef@19d7b43org.highwire.dtl.DTLVardef@79591org.highwire.dtl.DTLVardef@1ec805a_HPS_FORMAT_FIGEXP M_FIG C_FIG Mesenchymal stem cell membrane coated gelatin nanosphere as DDS nanocarrier

bioengineering↗

Direct Intercellular Vesicle Exchange between Adjacent Cells

Intercellular communication plays a central role in the development and integrity of multicellular organisms. Vesicle transfer, especially through extracellular space, has recently been highlighted as a critical intercellular communication modality, carrying nucleic acids, proteins, and others to distant cells. Previously, we demonstrated that extracellular vesicles induce "phenotypic synchronization of cells (PSyC)" during stem cell differentiation. While examining the mechanism underlying PSyC, we discovered a novel form of cellular communication mediated by direct intercellular vesicle exchange (DIVE) between adjacent cells across the plasma membrane (PM). By achieving cell-wide and high-spatiotemporal resolution imaging of vesicles labeled with fusion proteins of CD63 or CD81 to StayGold, a photostable fluorescent marker, we observed small vesicles (50-500 nm in diameter) directly transferred between adjacent cells. These vesicles moved at approximately 1 {micro}m/s and crossed PM in approximately 10-20 seconds. Furthermore, multiple vesicles traversed nearly identical sites of PM, suggesting the presence of specific routes or structures, potentially including a pore, mediating the vesicle transfer. Three-dimensional electron microscopy provided supportive observations for traversing vesicles with single membrane. These vesicles, named InterCellular Vesicles (InterCVs), were observed to colocalize with nucleic acids, including mRNA, microRNA, and DNA, suggesting the exchange of nucleic acid-mediated information, potentially inducing PSyC, between adjacent cells. Our discovery, DIVE, reveals a previously unknown modality of cell-cell communication, with the potential to reshape our understanding of cellular biology.

cell biology↗

Basic fibroblast growth factor helps protect facial nerve cells in a freeze-induced paralysis model

Severe axonal damage in the peripheral nerves results in retrograde degeneration towards the central side, leading to neuronal cell death, eventually resulting in incomplete axonal regeneration and functional recovery. Therefore, it is necessary to evaluate the facial nerve nucleus in models of facial paralysis and investigate the efficacy of treatments, to identify treatment options for severe paralysis. Consequently, we aimed to examine the percentage of facial nerve cell reduction and the extent to which intratympanic administration of a basic fibroblast growth factor (bFGF) inhibits neuronal cell death in a model of severe facial paralysis. A severe facial paralysis model was induced in Hartley guinea pigs by freezing the facial canal. Animals were divided into two groups: one group was treated with gelatin hydrogel impregnated with bFGF and the other was treated with saline. Facial movement scoring, electrophysiological testing, and histological assessment of facial neurons were performed at different postoperative time points. The freezing-induced facial paralysis model showed a facial neuronal cell death rate of 29.0%; however, bFGF administration reduced neuronal cell death to 15.8%. Facial movement scores also demonstrated improvement in the bFGF group compared with those in the control group. Intratympanic bFGF administration has a protective effect on facial neurons in a model of severe facial paralysis. These findings suggest a potential therapeutic approach for treating patients with refractory facial paralysis. Further studies are required to explore the clinical applicability of this treatment.

neuroscience↗

Metabolic intervention that reduces glucose-insulin signaling suppresses the onset and progression of neuroendocrine tumors

Insulin signaling often plays a role in the regulation of cancer including tumor initiation, progression, and response to treatment. In addition, the insulin-regulated PI3K-Akt-mTOR pathway plays an important role in the regulation of islet cell proliferation and this pathway is hyperactivated in human non-functional pancreatic neuroendocrine tumors (PanNETs). We therefore investigated the effect of a very low carbohydrate diet (ketogenic diet) on a mouse model that develops non-functional PanNETs to ask how reduced PI3K-Akt-mTOR signaling might affect the development and progression of non-functional PanNET. We found that this dietary intervention resulted in lower PI3K-Akt-mTOR signaling in islet cells and a significant reduction in PanNET formation and progression. We also found that this treatment had a significant effect on the suppression of pituitary NET development. Furthermore, we found that non-functional PanNET patients with lower blood glucose levels tend to have a better prognosis than patients with higher blood glucose levels. This preclinical study shows that a dietary intervention that results in lower serum insulin levels leads to lower insulin signal within the neuroendocrine cells and has a striking suppressive effect on the development and progression of both pancreatic and pituitary NETs.

cancer biology↗

Age-dependent decrease of hepatic geranylgeranoic acid and its oral supplementation prevents spontaneous hepatoma in C3H/HeN mice

AimGeranylgeranoic acid (GGA) has been developed as a preventive agent against second primary hepatoma. Recently, GGA was reported to induce cell death in human hepatoma cells via TLR4-mediated pyroptosis. We have reported that GGA is enzymatically biosynthesized from mevalonic acid in human hepatoma-derived cells and that endogenous GGA is found in most organs of rats. In addition, we found that upregulation of endogenous GGA levels by zaragozic acid A (ZAA) induced cell death in human hepatoma-derived cells. Therefore, we investigated the age-related changes of hepatic GGA and the possibility of suppressing hepatocarcinogenesis by GGA supplementation using male C3H/HeN mice that spontaneously develop hepatoma. MethodsWe measured endogenous GGA and mRNA of MAOB, a key enzyme of GGA biosynthesis, in the liver of male C3H/HeN mice aged 6-93 weeks. We also tried suppressing spontaneous hepatocarcinogenesis by a single administration of GGA to C3H/HeN mice. ResultsHepatic GGA content and Maob mRNA expression level age-dependently decreased in male C3H/HeN mice, some of which produced spontaneous hepatoma in 2 years. A single oral administration of GGA at 11 months of age significantly prevented hepatoma in terms of the number and weight of tumors per mouse at 23 months. Oral supplementation with GGA or geranylgeraniol significantly increased endogenous hepatic GGA contents dose-dependently, and ZAA dramatically upregulated hepatic GGA. ConclusionIn this study, we found an age-dependent decrease in hepatic endogenous GGA in male C3H/HeN mice and efficient prevention of spontaneous hepatoma by a single administration of GGA at 11 months of age.

cancer biology↗