Bismuth is a promising anodic for Li-ion batteries (LIBs) due to its adequate operating voltage and high-volume capacity (3,765 mAh cm-3). Nevertheless, inevitable volume expansion during Bi alloy reactions leads to severe capacity loss and cell destruction. To address this, a complex of bismuth alloy nanoparticles (Bi@NC) embedded in an N doping-carbon coating is fabricated via a simple pyrolysis method. Nano-sized bismuth alloys can improve the reaction dynamics through a shortened Li+-ion diffusion path. In addition, the N-doped carbon coating effectively buffers the volume change of bismuth during the extended alloy/dealloy reaction with Li+ ions and maintains an effective conductive network. Based on the Thermogravimetric analysis (TGA) showed high bismuth alloy loading (80.9 wt%) and maintained a high gravimetric capacity of 315 mAh g-1 up to 100 cycles with high volumetric capacity of 845.6 mAh cm-3.
The use of nanoparticles as a delivery system for a specific antigen could solve many limitations of mucosal vaccine applications, such as low immunogenicity, or antigen protection and stabilization. In this study, we tested the ability of nasally administered chitosan nanoparticles loaded with glycoprotein B of murine cytomegalovirus to induce an immune response in an animal model. The choice of chitosan nanoparticle type was made by in vitro evaluation of sorption efficiency and antigen release. Three types of chitosan nanoparticles were prepared: crosslinked with tripolyphosphate, coated with hyaluronic acid, and in complex with polycaprolactone. The hydrodynamic size of the nanoparticles by dynamic light scattering, zeta potential, Fourier transform infrared spectroscopy, scanning electron microscopy, stability, loading efficiency, and release kinetics with ovalbumin were evaluated. Balb/c mice were immunized intranasally using the three-dose protocol with nanoparticles, gB, and adjuvants Poly(I:C) and CpG ODN. Subsequently, the humoral and cell-mediated antigen-specific immune response was determined. On the basis of the properties of the tested nanoparticles, the cross-linked nanoparticles were considered optimal for further investigation. The results show that nanoparticles with Poly(I:C) and with gB alone raised IgG antibody levels above the negative control. In the case of mucosal IgA, only gB alone weakly induced the production of IgA antibodies compared to saline-immunized mice. The number of activated cells increased slightly in mice immunized with nanoparticles and gB compared to those immunized with gB alone or to negative control. The results demonstrated that chitosan nanoparticles could have potential in the development of mucosal vaccines.
The exocrine part of the pancreas has a duct system called the pancreatic ductal system (PDS). Its mechanism of development is complex, and any reorganization during early embryogenesis can give rise to anatomical variants. The aim of this study is to collect, classify, and analyze published evidence on the importance of anatomical variants of the PDS, addressing gaps in our understanding of such variations. The MEDLINE, Web of Science, Embase, and Google Scholar databases were searched to identify publications relevant to this review. R studio with meta-package was used for data extraction, risk of bias estimation, and statistical analysis. A total of 64 studies out of 1,778 proved suitable for this review and metanalysis. The meta-analysis computed the prevalence of normal variants of the PDS (92% of 10,514 subjects). Type 3 variants and "descending" subtypes of the main pancreatic duct (MPD) predominated in the pooled samples. The mean lengths of the MPD and accessory pancreatic duct (APD) were 16.53 cm and 3.36 cm, respectively. The mean diameters of the MPD at the head and the APD were 3.43 mm and 1.69 mm, respectively. The APD was present in only 41% of samples, and the long type predominated. The pancreatic ductal anatomy is highly variable, and the incorrect identification of variants may be challenging for surgeons during ductal anastomosis with gut, failure to which may often cause ductal obstruction or pseudocysts formation.
Jong Hyun Shin;Sun Ju Kim;Gwanghun Kim;Hang-Rae Kim;Kwan Soo Ko
Journal of Microbiology and Biotechnology
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v.34
no.10
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pp.2033-2040
/
2024
Deep learning presents a promising approach to complex biological classifications, contingent upon the availability of well-curated datasets. This study addresses the challenge of analyzing three-dimensional protein structures by introducing a novel pipeline that utilizes open-source tools to convert protein structures into a format amenable to computational analysis. Applying a two-dimensional convolutional neural network (CNN) to a dataset of 12,143 avian influenza virus genomes from 64 countries, encompassing 119 hemagglutinin (HA) and neuraminidase (NA) types, we achieved significant classification accuracy. The pathogenicity was determined based on the presence of H5 or H7 subtypes, and our models, ranging from zero to six mid-layers, indicated that a four-layer model most effectively identified highly pathogenic strains, with accuracies over 0.9. To enhance our approach, we incorporated Principal Component Analysis (PCA) for dimensionality reduction and one-class SVM for abnormality detection, improving model robustness through bootstrapping. Furthermore, the K-nearest neighbor (K-NN) algorithm was fine-tuned via hyperparameter optimization to corroborate the findings. The PCA identified distinct clustering for pathogenic HA, yielding an AUC of up to 0.85. The optimized K-NN model demonstrated an impressive accuracy between 0.96 and 0.97. These combined methodologies underscore our deep learning framework's capacity for rapid and precise identification of pathogenic avian influenza strains, thus providing a critical tool for managing global avian influenza threats.
Min Seok Woo;Eun-Jin Kim;Dong Kun Lee;Chung Eun Lee;Eun-A Ko;Dawon Kang
Journal of Animal Reproduction and Biotechnology
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v.39
no.2
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pp.81-87
/
2024
Background: Platelet-derived growth factor receptor alpha (PDGFRα) is essential for various biological processes, including fetal Leydig cell differentiation. The PDGFRαEGFP mouse model, which expresses an eGFP fusion gene under the native Pdgfrα promoter, serves as a valuable resource for exploring PDGFRα's expression and function in vivo. This study investigates PDGFRα expression in adult testicular cells using PDGFRαEGFP mouse model. Methods: Genotyping PCR and gel electrophoresis were used to confirm the zygosity of PDGFRαEGFP mice. Histological examination and fluorescence imaging were used to identify PDGFRα expression within testicular tissue. Immunohistochemical analysis assessed the co-expression of PDGFRα with c-Kit, ANO-1, and TASK-1 in testicular cells. Results: Genotyping confirmed the heterozygous status of the mice, which is crucial for studies due to the embryonic lethal phenotype observed in homozygotes. Histological and fluorescence imaging revealed that PDGFRα+ cells were primarily located in the interstitial spaces of the testis, specifically within Leydig cells and peritubular myoid cells (PMCs). Immunohistochemical results showed PDGFRα co-localization with c-Kit and ANO-1 in Leydig cells and a complete co-localization with TASK-1 in both Leydig cells and PMCs. Conclusions: The findings demonstrate specific expression of PDGFRα in Leydig cells and PMCs in adult testicular tissue. The co-expression of PDGFRα with c-Kit, ANO-1, and TASK-1 suggests complex regulatory mechanisms, possibly influencing testicular function and broader physiological processes.
Dong Uk Kim;Jehyun Nam;Matthew D. Cha;Sang‑Woo Kim
Oncology Letters
/
v.17
no.3
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pp.3589-3598
/
2019
Colorectal cancer (CRC) is a complex disease involving numerous genetic abnormalities. One of the major characteristics of CRC is enhanced Wnt signaling caused by loss-of-function mutations in the adenomatous polyposis coli (APC) gene. Previously, it has been demonstrated that the majority of malignant phenotypes following APC deletion in adult murine small intestines could be rescued when Myc, a downstream target of the Wnt pathway, was deleted. This indicated that Myc is a critical regulator of CRC development following APC loss. Previous studies reported that cyclic adenosine 3',5'-monophosphate (cAMP) can influence the AKT/mammalian target of rapamycin (mTOR) survival pathway in cancer and Myc is a critical downstream molecule of AKT/mTOR signaling. Phosphodiesterase 4D (PDE4D), a member of the cAMP-specific PDE4 family, has been associated with drug resistance in CRC. However, the association between PDE4D and Myc remains unclear. To investigate the potential role of PDE4D in Myc regulation in CRC, the present study evaluated the expression levels of PDE4 subtypes in DLD-1 CRC cells. Additionally, the effects of PDE4 inhibitors on Myc expression and oncogenic properties were analyzed by western blot analysis, reverse transcription-quantitative polymerase chain reaction, colony formation and soft agar assays. It was demonstrated that cAMP/PDE4D signals serve a critical role in regulating Myc expression in DLD-1 CRC cells. Furthermore, PDE4D was identified to be a main hydrolyzer of cAMP and suppression of PDE4D using selective inhibitors of PDE4 increased intracellular cAMP levels, which resulted in a marked decrease in the oncogenic properties of DLD-1 cells, including colony formation, cell proliferation and anchorage-independent growth. Notably, the current data imply that cAMP represses Myc expression via the downregulation of AKT/mTOR signaling, which was abolished by high PDE4D activities in DLD-1 cells. Additionally, a natural polyphenol resveratrol in combination with forskolin elevated the concentration of cAMP and enhanced the expression of Myc and the malignant phenotype of DLD-1 cells, reproducing the effect of known chemical inhibitors of PDE4. In conclusion, the present study identified that cAMP/PDE4D signaling is a critical regulator of Myc expression in DLD-1 and possibly other CRC cells.
Lupus is characterized by the autoantibodies against nuclear Ags, underscoring the importance of identifying the B cell subsets driving autoimmunity. Our research focused on the mitochondrial activity and CXCR4 expression in CD11c+ B cells from lupus patients after ex vivo stimulation with a TLR9 agonist, CpG-oligodeoxyribonucleotide (ODN). We also evaluated the response of CD11c+ B cells in ODN-injected mice. Post-ex vivo ODN stimulation, we observed an increase in the proportion of CD11chi cells, with elevated mitochondrial activity and CXCR4 expression in CD11c+ B cells from lupus patients. In vivo experiments showed similar patterns, with TLR9 stimulation enhancing mitochondrial and CXCR4 activities in CD11chi B cells, leading to the generation of anti-dsDNA plasmablasts. The CXCR4 inhibitor AMD3100 and the mitochondrial complex I inhibitor IM156 significantly reduced the proportion of CD11c+ B cells and autoreactive plasmablasts. These results underscore the pivotal roles of mitochondria and CXCR4 in the production of autoreactive plasmablasts.
Spinal cord injury (SCI) is a serious nervous system disease that usually leads to the impairment of the motor, sensory, and autonomic nervous functions of the spinal cord, and it places a heavy burden on families and healthcare systems every year. Due to the complex pathophysiological mechanism of SCI and the poor ability of neurons to regenerate, the current treatment scheme has very limited effects on the recovery of spinal cord function. In addition, due to their unique advantages, exosomes can be used as carriers for cargo transport. In recent years, some studies have confirmed that treatment with mesenchymal stem cells (MSCs) can promote the recovery of SCI nerve function. The therapeutic effect of MSCs is mainly related to exosomes secreted by MSCs, and exosomes may have great potential in SCI therapy. In this review, we summarized the repair mechanism of mesenchymal stem cells-derived exosomes (MSCs-Exos) in SCI treatment and discussed the microRNAs related to SCI treatment based on MSCs-Exos and their mechanism of action, which is helpful to further understand the role of exosomes in SCI.
This study was performed to investigate the distribution and differentiation on the immunoreacted cells of the ChAT (choline acetyltransferase) at the Meynert basal nucleus of the forebrains in the growth periods of rat, using the immunohistochemistric method. According to the cell shape and the ratio of long axis vs short axis of cell soma, the ChAT antibody reacted nerve cells in the Meynert basal nucleus of the rats were classified into six types. In the adult rats, the FD (frequency distributions) of round, oval and elongated cells were maximum. The FD of these types were shown to be progressively decreased during the postnatal development. In addition, the FD of elongated nerve cells in were observed in the adult rats respectively. This was thought to be the same phenomenon as those in the round and oval cells . The total mean volume of ChAT antibody reacted cell somata was lowest in the PND (postnatal days) 7 rats and was highest in the PND 21 rats. But, those were decreased to the adult. These results suggest that ChAT antibody reacted nerve cells grow up to PND 21 and then, differentiate into the various types by neurites outgrowing. On the electron micrography, the adult rat forebrain cells were obtained to be well developed ribosomes, polysomes , rough endoplasmic reticula and mitochondria. The immunreactivities were observed in ribosomes, polysomes, rough endoplasmic reticula and outer membrane of mitochondria. Golgi complexes were poorly developed and not showed jmmunreactivity. The ribosomes , polysomes and endoplasmic reticula are considered to be closely related to the inter cellular localization and biosynthesis of the ChAT but not Golgi complex. According to the results in the present study, it is considered that the ChAT-immunoreacted nerve cells in the Meynert basal nucleus of the rat forebrains are differentiated throughout the postnatal development with following processes of changes; 1) the cholinergic nerve cells develop postnatally 2) cell soma volumes gradually increase during the early postnatal days 3) and then, cells differentiate into the various types by projecting the neurites to the appropriate area after PND 21.
No, Hoon-Jeong;Moon, Gu;Moon, Seok-Jae;Won, Jin-Hee;Moon, Young-Ho;Park, Rae-Gil
THE JOURNAL OF KOREAN ORIENTAL ONCOLOGY
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v.6
no.1
/
pp.81-97
/
2000
Objectives: This experimental study was carried out to evaluate the effects of aqueous and methanol extracts of Hedyotis diffusa which has long been used for cancer treatment in oriental medicines on the induction of apoptotic cell death in human lymphoid leukemia cell line, HL-60. Methods: Cells were treated with various concentrations (200 to $0.4{\mu}g$) and periods (6 to 30 hr) of $H_2O$ and methanol extracts of Hedyotis diffusa. Then, cells were tested for viability by MTT assay. Cells wrere treated with $200{\mu}g/ml$ of methanol extract fork various periods. Genomic DNA was isolated, separated, on 1.5% agarose gels, stained with ethidium bromide and visualized under UV light. Cells were treated with $200{\mu}g/ml$ of each extract for 16 hr. Then, cells were treated with Hoechst dye 33342 and observed by fluorescence microscopy. Cells were treated with various doses of each for 12 hr and $100{\mu}g/ml$ of methanol extract for various periods. Lysate from the cells used to measure the activity of Caspase-1 and-3 proteases by using fluorogenic peptide substrates including acetyl-YVAD-AMC and acetyl-DEVD-AMC, respectively. Cells were treated with $200{\mu}g/ml$ of each extract for various periods. Cell lysates were immunoprecipated with anti-JNKl antibodies. The immune complex was reacted with $32^p-ATP$ and c-Jun as a substrate. The phosphotransferase activity of JNKI was measured by using PhosphoImage analyzer (Fuji Co., Japan). Nuclear extracts were isolated and incubated with oligonucleotide probe of $NF-{\kappa}B$. Transcriptional activation of ${\kappa}B$ was measured by using EMSA and visualized by PhosphoImage analyzer (Fuji Co, Japan). Cell lysates were prepared and analyzed by Western blotting with anti-Bc12 antibodies and anti-Bax antibodies. Cells were pretreated with various doses of methanol extract for 2 hr. Then, the extract was removed by centrifugation. Cells were resuspended with RPMI-1640 media containing 0.3% agarose, 10% FBS, overlayred onto bottom layer agarose and incubated at $CO_2$ incubator for 6 days. The number of colony was counted under light microscopy ($\time100$). Results: The death of HL-60 cells was markedly induced by the addition of methanol extract of Hedyotis diffusa in a dose and time-dependent manners. The apoptotic characteristic ladder pattern of DNA strand break was observed in death of HL-60 cells. In addition, it was shown nucleus chromatin condensation and fragmentation under Hoechst staining. Therefore, Hedyotis diffusa extract-induced death of HL-60 cells is mediated by apoptotic signaling processes. The activity of Caspase 3-like proteases remained in a basal level in HL-60 cells treated with aqueous extract of Hedyotis diffusa. However, it was markedly increased in HL-60 cells treated with methanol extract of Hedyotis diffusa. In addition, the phosphotransferase activity of JNKl was increased in HL-60 cells treated with methanol extract of Hedyotis diffusa. Furthermore, the activation of transcriptional activator, $NF-{\kappa}B$ was markedly induced by methanol extract of Hedyotis diffusa. Anti-apoptotic Bc12 was cleaved into 23Kda fragment by treatment of methanol extract of Hedyotis diffusa. However, expression of proapoptotic Bax protein was increased by treatment of methanol extract of Hedyotis diffusa in a time-dependent manner. Furthermore, methanol extract markedly inhibited the colony forming efficiency of HL-60 cells in semisolid agar culture. Conclusions: Above results suggest that methanol extract of Hedyotis diffusa induces the apoptotic death of human leukemic HL-60 cells via activations of Caspase-3 proteases, JNKI, transcriptional activator $NF-{\kappa}B$, In addition, our results also suggest that methanol extract of Hedyotis diffusa reduces the malignant potential of HL-60 cells via down regulation of colony forming effciency through cleavage of Bc12 as well as induction of Bax.
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