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  • 1
    Online Resource
    Online Resource
    Production of Bivalent Subunit Vaccine for Porcine via 2A-Like Sequence in Baculovirus Expression Vector System
    MDPI AG ; 2022
    In:  Processes Vol. 10, No. 5 ( 2022-05-01), p. 895-
    Details
    In: Processes, MDPI AG, Vol. 10, No. 5 ( 2022-05-01), p. 895-
    Abstract: Classical swine fever virus (CSFV) and porcine circovirus type 2 (PCV2) have caused severe diseases in swine populations worldwide. Here, a polycistronic baculovirus vector was developed to express a bivalent vaccine, consisting of the CSFV-E2 and PCV2-Cap protein, and an immunomodulator protein derived from the Flammulina velutipes, FVE-FIP, as well as the selection marker, green fluorescent protein. The simultaneous expression of the CSFV-E2 and PCV2-Cap protein was mediated by the 2A-like sequence derived from the Perina nuda virus (PnV), while the expression of the FVE-FIP was driven by the internal ribosome entry site (IRES) element derived from the Rhophalosipum padi virus (RhPV). The Western blot analysis result suggested that the CSFV-E2, PCV2-Cap, and FVE-FIP protein were successfully co-expressed by the infected Spodoptera frugiperda IPBL-Sf21 (Sf21) cell line. The extracted cell lysate containing all three recombinant proteins was administered to Balb/C mice with or without the supplementation of Freund’s adjuvant. The ELISA analysis of the serum collected from all the immunized groups showed detectable antibodies against CSFV-E2 and PCV2-Cap. Furthermore, the immunized group without the adjuvant supplementation demonstrated a similar level of antibodies to the group with adjuvant supplementation, suggesting the efficiency of the FVE-FIP in enhancing the immune response. These results demonstrated the polycistronic baculovirus vector could be employed to develop bivalent vaccines for pigs.
    Type of Medium: Online Resource
    ISSN: 2227-9717
    URL: Article
    DOI: 10.3390/pr10050895
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2720994-5
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  • 2
    Online Resource
    Online Resource
    Chlorella sorokiniana Extract Prevents Cisplatin-Induced Myelotoxicity In Vitro and In Vivo
    Hindawi Limited ; 2020
    In:  Oxidative Medicine and Cellular Longevity Vol. 2020 ( 2020-01-25), p. 1-14
    Details
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2020 ( 2020-01-25), p. 1-14
    Abstract: Cisplatin chemotherapy causes myelosuppression and often limits treatment duration and dose escalation in patients. Novel approaches to circumvent or lessen myelotoxicity may improve clinical outcome and quality of life in these patients. Chlorella sorokiniana (CS) is a freshwater unicellular green alga and exhibits encouraging efficacy in immunomodulation and anticancer in preclinical studies . However, the efficacy of CS on chemoprotection remains unclear. We report here, for the first time, that CS extract (CSE) could protect normal myeloid cells and PBMCs from cisplatin toxicity. Also, cisplatin-induced apoptosis in HL-60 cells was rescued through reservation of mitochondrial function, inhibition of cytochrome c release to cytosol, and suppression of caspase and PARP activation. Intriguingly, cotreatment of CSE attenuated cisplatin-evoked hypocellularity of bone marrow in mice. Furthermore, we observed the enhancement of CSF-GM activity in bone marrow and spleen in mice administered CSE and cisplatin, along with increased CD11b levels in spleen. In conclusion, we uncovered a novel mechanism of CSE on myeloprotection, whereby potentially supports the use of CSE as a chemoprotector against cisplatin-induced bone marrow toxicity. Further clinical investigation of CSE in combination with cisplatin is warranted.
    Type of Medium: Online Resource
    ISSN: 1942-0900 , 1942-0994
    URL: Article
    DOI: 10.1155/2020/7353618
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2020
    detail.hit.zdb_id: 2455981-7
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  • 3
    Online Resource
    Online Resource
    Neuroprotective Effects of a Multi-Herbal Extract on Axonal and Synaptic Disruption in Vitro and Cognitive Impairment in Vivo
    IOS Press ; 2023
    In:  Journal of Alzheimer's Disease Reports Vol. 7, No. 1 ( 2023-01-27), p. 51-76
    Details
    In: Journal of Alzheimer's Disease Reports, IOS Press, Vol. 7, No. 1 ( 2023-01-27), p. 51-76
    Abstract: Background: Alzheimer’s disease (AD) is a multifactorial disorder characterized by cognitive decline. Current available therapeutics for AD have limited clinical benefit. Therefore, preventive therapies for interrupting the development of AD are critically needed. Molecules targeting multifunction to interact with various pathlogical components have been considered to improve the therapeutic efficiency of AD. In particular, herbal medicines with multiplicity of actions produce cognitive benefits on AD. Bugu-M is a multi-herbal extract composed of Ganoderma lucidum (Antler form), Nelumbo nucifera Gaertn., Ziziphus jujuba Mill., and Dimocarpus longan, with the ability of its various components to confer resilience to cognitive deficits. Objective: To evaluate the potential of Bugu-M on amyloid-β (Aβ) toxicity and its in vitro mechanisms and on in vivo cognitive function. Methods: We illustrated the effect of Bugu-M on Aβ25–35-evoked toxicity as well as its possible mechanisms to diminish the pathogenesis of AD in rat cortical neurons. For cognitive function studies, 2-month-old female 3×Tg-AD mice were administered 400 mg/kg Bugu-M for 30 days. Behavioral tests were performed to assess the efficacy of Bugu-M on cognitive impairment. Results: In primary cortical neuronal cultures, Bugu-M mitigated Aβ-evoked toxicity by reducing cytoskeletal aberrations and axonal disruption, restoring presynaptic and postsynaptic protein expression, suppressing mitochondrial damage and apoptotic signaling, and reserving neurogenic and neurotrophic factors. Importantly, 30-day administration of Bugu-M effectively prevented development of cognitive impairment in 3-month-old female 3×Tg-AD mice. Conclusion: Bugu-M might be beneficial in delaying the progression of AD, and thus warrants consideration for its preventive potential for AD.
    Type of Medium: Online Resource
    ISSN: 2542-4823
    URL: Article
    DOI: 10.3233/ADR-220056
    Language: Unknown
    Publisher: IOS Press
    Publication Date: 2023
    detail.hit.zdb_id: 2955863-3
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  • 4
    Online Resource
    Online Resource
    A novel in-frame GFAP p.E138_L148del mutation in Type II Alexander disease with atypical phenotypes
    Springer Science and Business Media LLC ; 2022
    In:  European Journal of Human Genetics Vol. 30, No. 6 ( 2022-06), p. 687-694
    Details
    In: European Journal of Human Genetics, Springer Science and Business Media LLC, Vol. 30, No. 6 ( 2022-06), p. 687-694
    Type of Medium: Online Resource
    ISSN: 1018-4813 , 1476-5438
    URL: Article
    DOI: 10.1038/s41431-022-01073-2
    RVK:
    XA 10000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2005160-8
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    Elevated GFAP isoform expression promotes protein aggregation and compromises astrocyte function
    Wiley ; 2021
    In:  The FASEB Journal Vol. 35, No. 5 ( 2021-05)
    Details
    In: The FASEB Journal, Wiley, Vol. 35, No. 5 ( 2021-05)
    Type of Medium: Online Resource
    ISSN: 0892-6638 , 1530-6860
    URL: Issue
    URL: Article
    DOI: 10.1096/fsb2.v35.5
    DOI: 10.1096/fj.202100087R
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 1468876-1
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Effects of Alexander disease–associated mutations on the assembly and organization of GFAP intermediate filaments
    American Society for Cell Biology (ASCB) ; 2022
    In:  Molecular Biology of the Cell Vol. 33, No. 8 ( 2022-07-01)
    Details
    In: Molecular Biology of the Cell, American Society for Cell Biology (ASCB), Vol. 33, No. 8 ( 2022-07-01)
    Abstract: Alexander disease is a primary genetic disorder of astrocytes caused by dominant mutations in the gene encoding glial fibrillary acidic protein (GFAP). How single-amino-acid changes can lead to cytoskeletal catastrophe and brain degeneration remains poorly understood. In this study, we have analyzed 14 missense mutations located in the GFAP rod domain to investigate how these mutations affect in vitro filament assembly. Whereas the internal rod mutants assembled into filaments that were shorter than those of wild type, the rod end mutants formed structures with one or more of several atypical characteristics, including short filament length, irregular width, roughness of filament surface, and filament aggregation. When transduced into primary astrocytes, GFAP mutants with in vitro assembly defects usually formed cytoplasmic aggregates, which were more resistant to biochemical extraction. The resistance of GFAP to solubilization was also observed in brain tissues of patients with Alexander disease, in which a significant proportion of insoluble GFAP were accumulated in Rosenthal fiber fractions. These findings provide clinically relevant evidence that link GFAP assembly defects to disease pathology at the tissue level and suggest that altered filament assembly and properties as a result of GFAP mutation are critical initiating factors for the pathogenesis of Alexander disease.
    Type of Medium: Online Resource
    ISSN: 1059-1524 , 1939-4586
    URL: Article
    DOI: 10.1091/mbc.E22-01-0013
    Language: English
    Publisher: American Society for Cell Biology (ASCB)
    Publication Date: 2022
    detail.hit.zdb_id: 1474922-1
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Recessively‐Inherited Adult‐Onset Alexander Disease Caused by a Homozygous Mutation in the GFAP Gene
    Wiley ; 2020
    In:  Movement Disorders Vol. 35, No. 9 ( 2020-09), p. 1662-1667
    Details
    In: Movement Disorders, Wiley, Vol. 35, No. 9 ( 2020-09), p. 1662-1667
    Abstract: Alexander disease (AxD) is an autosomal‐dominant leukodystrophy caused by heterozygous mutations in the glial fibrillary acidic protein ( GFAP ) gene. Objectives The objective of this report is to characterize the clinical phenotype and identify the genetic mutation associated with adult‐onset AxD. Methods A man presented with progressive unsteadiness since age 16. Magnetic resonance imaging findings revealed characteristic features of AxD. The GFAP gene was screened, and a candidate variant was functionally tested to evaluate causality. Results A homozygous c.197G  〉  A (p.Arg66Gln) mutation was found in the proband, and his asymptomatic parents were heterozygous for the same mutation. This mutation affected GFAP solubility and promoted filament aggregation. The presence of the wild‐type protein rescued mutational effects, consistent with the recessive nature of this mutation. Conclusions This study is the first report of AxD caused by a homozygous mutation in GFAP . The clinical implication is while examining patients with characteristic features on suspicion of AxD, GFAP screening is recommended even without a supportive family history. © 2020 International Parkinson and Movement Disorder Society
    Type of Medium: Online Resource
    ISSN: 0885-3185 , 1531-8257
    URL: Issue
    URL: Article
    DOI: 10.1002/mds.v35.9
    DOI: 10.1002/mds.28099
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2041249-6
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  • 8
    Online Resource
    Online Resource
    Antisense therapy in a rat model of Alexander disease reverses GFAP pathology, white matter deficits, and motor impairment
    American Association for the Advancement of Science (AAAS) ; 2021
    In:  Science Translational Medicine Vol. 13, No. 620 ( 2021-11-17)
    Details
    In: Science Translational Medicine, American Association for the Advancement of Science (AAAS), Vol. 13, No. 620 ( 2021-11-17)
    Abstract: Alexander disease (AxD) is a devastating leukodystrophy caused by gain-of-function mutations in GFAP , and the only available treatments are supportive. Recent advances in antisense oligonucleotide (ASO) therapy have demonstrated that transcript targeting can be a successful strategy for human neurodegenerative diseases amenable to this approach. We have previously used mouse models of AxD to show that Gfap -targeted ASO suppresses protein accumulation and reverses pathology; however, the mice have a mild phenotype with no apparent leukodystrophy or overt clinical features and are therefore limited for assessing functional outcomes. In this report, we introduce a rat model of AxD that exhibits hallmark pathology with GFAP aggregation in the form of Rosenthal fibers, widespread astrogliosis, and white matter deficits. These animals develop normally during the first postnatal weeks but fail to thrive after weaning and develop severe motor deficits as they mature, with about 14% dying of unknown cause between 6 and 12 weeks of age. In this model, a single treatment with Gfap -targeted ASO provides long-lasting suppression, reverses GFAP pathology, and, depending on age of treatment, prevents or mitigates white matter deficits and motor impairment. In this report, we characterize an improved animal model of AxD with myelin pathology and motor impairment, recapitulating prominent features of the human disease, and use this model to show that ASO therapy has the potential to not only prevent but also reverse many aspects of disease.
    Type of Medium: Online Resource
    ISSN: 1946-6234 , 1946-6242
    URL: Article
    DOI: 10.1126/scitranslmed.abg4711
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2021
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  • 9
    Online Resource
    Online Resource
    The Behavior of Self-Monitoring of Blood Glucose and Glycemic Control in Taiwanese Population
    MDPI AG ; 2022
    In:  Endocrines Vol. 3, No. 2 ( 2022-05-06), p. 214-222
    Details
    In: Endocrines, MDPI AG, Vol. 3, No. 2 ( 2022-05-06), p. 214-222
    Abstract: Self-monitoring of blood glucose (SMBG) is common in patients with diabetes. The aim of this study was to explore how frequency/behavior of SMBG affect glucose control in patients with type 2 diabetes. This cross-sectional study was conducted at a regional teaching hospital in Taiwan. All participants completed a structured questionnaire about the frequency and behavior of SMBG, and hemoglobulin A1C (A1C) data were recorded from medical records. A total of 382 diabetes outpatients participated in the study. In the patients using insulin injections, A1C was better in patients with SMBG ≥ 28 times than in those with SMBG 〈 28 times per month (7.82 ± 1.86% vs. 8.33 ± 1.31%, p = 0.025). In the patients not using insulin, A1C was better in patients with SMBG 〉 14 times than those with SMBG ≤ 14 times per month (7.08 ± 0.23% vs. 7.55 ± 0.08%, p = 0.038). The patients who more frequently reviewed the causes of hypoglycemia and hyperglycemia had a better A1C level (p for linear trend 〈 0.001). Our study suggested that SMBG ≥ 28 and 〉 14 times could improve glycemic control for insulin-requiring and non-insulin-requiring type 2 diabetes patients, respectively. Further exploration of the cause of hyperglycemia or hypoglycemia shown by SMBG could also improve blood glucose control.
    Type of Medium: Online Resource
    ISSN: 2673-396X
    URL: Article
    DOI: 10.3390/endocrines3020019
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 3019981-5
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  • 10
    Online Resource
    Online Resource
    The Relationship between Obesity-Related Factors and Graves’ Orbitopathy: A Pilot Study
    MDPI AG ; 2022
    In:  Medicina Vol. 58, No. 12 ( 2022-11-29), p. 1748-
    Details
    In: Medicina, MDPI AG, Vol. 58, No. 12 ( 2022-11-29), p. 1748-
    Abstract: Background and Objectives: The aim of this study was to investigate the relationships between obesity-related factors including body mass index (BMI), diabetes or prediabetes, hyperlipidemia, fasting plasma glucose, fasting plasma insulin, homeostasis model assessment-estimated insulin resistance (HOMA-IR), highly sensitive C-reactive protein (hs-CRP) and Graves’ orbitopathy (GO). Materials and Methods: Eighty-four patients with Graves’ disease (GD) (42 without GO and 42 with GO) were enrolled in this cross-sectional cohort study. Gender, age, GD treatment history, height, body weight, waist circumference, smoking status, co-morbidities, levels of free thyroxin, thyroid-stimulating hormone, thyroid-stimulating hormone receptor (TSHR) antibodies, fasting plasma glucose and insulin, and hs-CRP were recorded. The eye condition was evaluated using the consensus statement of the European Group of Graves’ Orbitopathy (EUGOGO) and the NOSPECS classification. Results: In this study, multivariate regression analysis showed that BMI, fasting plasma insulin, and HOMA-IR were associated with the presence of GO after adjusting the age, gender, smoking, TSHR antibodies, and steroid usage (adjusted odd’s ratio (aOR) 1.182, 95% confidence interval (95% CI), 1.003–1.393, p = 0.046; aOR 1.165, 95% CI, 1.001–1.355, p = 0.048; and aOR 1.985, 95% CI, 1.046–3.764, p = 0.036, respectively). In addition, BMI, fasting plasma glucose, fasting plasma insulin, HOMA-IR, and hs-CRP levels were positively correlated with the severity of GO. Conclusions: The findings of this study suggest that obesity-related factors, especially fasting plasma insulin and HOMA-IR, are related to GO. Our study highlighted the importance of obesity-related factors in GO. Obesity-related factors may cause the development of GO or occur simultaneously with GO.
    Type of Medium: Online Resource
    ISSN: 1648-9144
    URL: Article
    DOI: 10.3390/medicina58121748
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2088820-X
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