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  • 1
    In: Frontiers in Genetics, Frontiers Media SA, Vol. 14 ( 2023-9-21)
    Abstract: With the increasing throughput of modern sequencing instruments, the cost of storing and transmitting sequencing data has also increased dramatically. Although many tools have been developed to compress sequencing data, there is still a need to develop a compressor with a higher compression ratio. We present a two-step framework for compressing sequencing data in this paper. The first step is to repack original data into a binary stream, while the second step is to compress the stream with a LZMA encoder. We develop a new strategy to encode the original file into a LZMA highly compressed stream. In addition an FPGA-accelerated of LZMA was implemented to speedup the second step. As a demonstration, we present repaq as a lossless non-reference compressor of FASTQ format files. We introduced a multifile redundancy elimination method, which is very useful for compressing paired-end sequencing data. According to our test results, the compression ratio of repaq is much higher than other FASTQ compressors. For some deep sequencing data, the compression ratio of repaq can be higher than 25, almost four times of Gzip. The framework presented in this paper can also be applied to develop new tools for compressing other sequencing data. The open-source code of repaq is available at: https://github.com/OpenGene/repaq .
    Type of Medium: Online Resource
    ISSN: 1664-8021
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2606823-0
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  • 2
    In: Biomolecules, MDPI AG, Vol. 11, No. 2 ( 2021-02-08), p. 238-
    Abstract: Chimeric antigen receptor (CAR) T therapy represents a form of immune cellular therapy with clinical efficacy and a specific target. A typical chimeric antigen receptor (CAR) construct consists of an antigen binding domain, a transmembrane domain, and a cytoplasmic domain. Nanobodies have been widely applied as the antigen binding domain of CAR-T due to their small size, optimal stability, high affinity, and manufacturing feasibility. The nanobody-based CAR structure has shown a proven function in more than ten different tumor-specific targets. After being transduced in Jurkat cells, natural killer cells, or primary T cells, the resulting nanobody-based CAR-T or CAR-NK cells demonstrate anti-tumor effects both in vitro and in vivo. Interestingly, anti-BCMA CAR-T modulated by a single nanobody or bi-valent nanobody displays comparable clinical effects with that of single-chain variable fragment (scFv)-modulated CAR-T. The application of nanobodies in CAR-T therapy has been well demonstrated from bench to bedside and displays great potential in forming advanced CAR-T for more challenging tasks.
    Type of Medium: Online Resource
    ISSN: 2218-273X
    Language: English
    Publisher: MDPI AG
    Publication Date: 2021
    detail.hit.zdb_id: 2701262-1
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  • 3
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Circulation Research Vol. 118, No. 3 ( 2016-02-05), p. 388-399
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 118, No. 3 ( 2016-02-05), p. 388-399
    Abstract: Aortic aneurysm is a life-threatening cardiovascular disorder caused by the predisposition for dissection and rupture. Genetic studies have proved the involvement of the transforming growth factor-β (TGF-β) pathway in aortic aneurysm. Smad4 is the central mediator of the canonical TGF-β signaling pathway. However, the exact role of Smad4 in smooth muscle cells (SMCs) leading to the pathogenesis of aortic aneurysms is largely unknown. Objective: To determine the role of smooth muscle Smad4 in the pathogenesis of aortic aneurysms. Methods and Results: Conditional gene knockout strategy combined with histology and expression analysis showed that Smad4 or TGF-β receptor type II deficiency in SMCs led to the occurrence of aortic aneurysms along with an upregulation of cathepsin S and matrix metallopeptidase-12, which are proteases essential for elastin degradation. We further demonstrated a previously unknown downregulation of matrix metallopeptidase-12 by TGF-β in the aortic SMCs, which is largely abrogated in the absence of Smad4. Chemotactic assay and pharmacologic treatment demonstrated that Smad4-deficient SMCs directly triggered aortic wall inflammation via the excessive production of chemokines to recruit macrophages. Monocyte/macrophage depletion or blocking selective chemokine axis largely abrogated the progression of aortic aneurysm caused by Smad4 deficiency in SMCs. Conclusions: The findings reveal that Smad4-dependent TGF-β signaling in SMCs protects against aortic aneurysm formation and dissection. The data also suggest important implications for novel therapeutic strategies to limit the progression of the aneurysm resulting from TGF-β signaling loss-of-function mutations.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 1467838-X
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  • 4
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2005
    In:  Circulation Research Vol. 97, No. 8 ( 2005-10-14), p. 821-828
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 97, No. 8 ( 2005-10-14), p. 821-828
    Abstract: Transforming growth factor-βs (TGF-βs) are pleiotropic cytokines involved in many physiological and pathological processes, including heart development and heart disease. Smad4 is the central intracellular mediator of TGF-β signaling. To investigate the function of Smad4 in heart development further, we generated a strain of cardiomyocyte-specific Smad4 knockout mice using the Cre– lox P system. Unexpectedly, the deletion of Smad4 in cardiomyocytes resulted in cardiac hypertrophy characterized by an increase in the size of cardiac myocytes, age-associated fibrosis, and reexpression of certain fetal genes. Approximately 70% of the Smad4 mutant mice died spontaneously between 5 and 12 months of age. Echocardiography and an invasive hemodynamic study of the left ventricle revealed markedly decreased cardiac contractility in Smad4 mutant mice compared with littermate controls. Moreover, phosphorylated extracellular signal–regulated kinase (ERK) 1/2 and mitogen-activated protein kinase–ERK (MEK) 1 were increased in the Smad4 mutants, suggesting that an upregulation of MEK1–ERK1/2 signaling as a consequence of deletion of Smad4 underlies the impaired cardiac function. These results reveal an important function of Smad4 in cardiac remodeling and suggest that an altered cellular response to TGF-β could be a mechanism by which cardiac myocytes undergo hypertrophy.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2005
    detail.hit.zdb_id: 1467838-X
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  • 5
    In: Viruses, MDPI AG, Vol. 14, No. 5 ( 2022-05-14), p. 1046-
    Abstract: Herpes simplex virus type 1 (HSV-1), an α subgroup member of the human herpesvirus family, infects cells via the binding of its various envelope glycoproteins to cellular membrane receptors, one of which is herpes virus entry mediator (HVEM), expressed on dendritic cells. Here, HVEM gene-deficient mice were used to investigate the immunologic effect elicited by the HSV-1 infection of dendritic cells. Dendritic cells expressing the surface marker CD11c showed an abnormal biological phenotype, including the altered transcription of various immune signaling molecules and inflammatory factors associated with innate immunity after viral replication. Furthermore, the viral infection of dendritic cells interfered with dendritic cell function in the lymph nodes, where these cells normally play roles in activating the T-cell response. Additionally, the mild clinicopathological manifestations observed during the acute phase of HSV-1 infection were associated with viral replication in dendritic cells.
    Type of Medium: Online Resource
    ISSN: 1999-4915
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2516098-9
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  • 6
    Online Resource
    Online Resource
    Frontiers Media SA ; 2021
    In:  Frontiers in Cell and Developmental Biology Vol. 9 ( 2021-10-25)
    In: Frontiers in Cell and Developmental Biology, Frontiers Media SA, Vol. 9 ( 2021-10-25)
    Abstract: Background: Lung cancer is the leading cause of cancer-related death worldwide, of which lung adenocarcinoma (LUAD) is one of the main histological subtypes. Mitochondria are vital for maintaining the physiological function, and their dysfunction has been found to be correlated with tumorigenesis and disease progression. Although, some mitochondrial-related genes have been found to correlate with the clinical outcomes of multiple tumors solely. The integrated relationship between nuclear mitochondrial genes (NMGs) and the prognosis of LUAD remains unclear. Methods: The list of NMGs, gene expression data, and related clinical information of LUAD were downloaded from public databases. Bioinformatics methods were used and obtained 18 prognostic related NMGs to construct a risk signature. Results: There were 18 NMGs ( NDUFS2 , ATP8A2 , SCO1 , COX14 , COA6 , RRM2B , TFAM , DARS2 , GARS , YARS2 , EFG1 , GFM1 , MRPL3 , MRPL44 , ISCU , CABC1 , HSPD1 , and ETHE1 ) identified by LASSO regression analysis. The mRNA expression of these 18 genes was positively correlated with their relative linear copy number alteration (CNA). Meanwhile, the established risk signature could effectively distinguish high- and low-risk patients, and its predictive capacity was validated in three independent gene expression omnibus (GEO) cohorts. Notably, a significantly lower prevalence of actionable EGFR alterations was presented in patients with high-risk NMGs signature but accompanied with a more inflame immune tumor microenvironment. Additionally, multicomponent Cox regression analysis showed that the model was stable when risk score, tumor stage, and lymph node stage were considered, and the 1-, 3-, and 5-year AUC were 0.74, 0.75, and 0.70, respectively. Conclusion: Together, this study established a signature based on NMGs that is a prognostic biomarker for LUAD patients and has the potential to be widely applied in future clinical settings.
    Type of Medium: Online Resource
    ISSN: 2296-634X
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2737824-X
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  • 7
    In: Nanoscale, Royal Society of Chemistry (RSC), Vol. 14, No. 3 ( 2022), p. 976-983
    Abstract: Azobenzenes are great photochromic molecules for switching the physical properties of various materials via trans – cis isomerization. However, the UV light resulted cis -azobenzene is metastable and thermodynamically gets back to trans -azobenzene after ceasing UV irradiation, which causes an unwanted property change of azobenzene-containing materials. Additionally, thermal and mechanical conditions would accelerate this process dramatically. In this present work, a new type of azobenzene-containing surfactant is designed for the fabrication of photoresponsive phase change biomaterials. With a “locked” cis -azobenzene conformation, the resulting biomaterials could maintain their disordered state after ceasing UV light, which exhibit great resistance to thermal and piezo conditions. Interestingly, the “locked” cis -azobenzene could be unlocked by Vis light in high efficiency, which opens a new way for the design of phase change materials only responding to light. By showing stable cis -azobenzene maintained physical state, the newly fabricated biomaterials provide new potential for the construction of advanced materials, like self-healing materials, with less use of long time UV irradiation for maintaining their disordered states.
    Type of Medium: Online Resource
    ISSN: 2040-3364 , 2040-3372
    Language: English
    Publisher: Royal Society of Chemistry (RSC)
    Publication Date: 2022
    detail.hit.zdb_id: 2515664-0
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  • 8
    Online Resource
    Online Resource
    Royal Society of Chemistry (RSC) ; 2022
    In:  Materials Chemistry Frontiers Vol. 6, No. 15 ( 2022), p. 2122-2127
    In: Materials Chemistry Frontiers, Royal Society of Chemistry (RSC), Vol. 6, No. 15 ( 2022), p. 2122-2127
    Abstract: Lignin is one of the abundant natural biomass resources. Developing lignin into fluorescent materials is gaining continuous attraction. In this study, a type of fluorescent lignin ionic complexes (LS-TPEA) is developed via the electrostatic complexation between ligninsulfonate and a tetraphenylethene-containing ammonium surfactant. The solvent-free LS-TPEA materials show thermotropic liquid crystal properties, and could exhibit blue luminescence under UV light. The fluorescence emission of LS-TPEA relies on the ordered structure, which could be turned off by forming isotropic liquid. The good thermostability allows LS-TPEA to be recyclable labeling biomaterials suitable for working at high temperatures, and by taking advantage of the water-resistance properties LS-TPEA would also be good hydrophobic fluorescent coating materials. This work provides a designing strategy for fabricating fluorescent lignin materials, facilitating the value-added utilization of lignin resources.
    Type of Medium: Online Resource
    ISSN: 2052-1537
    Language: English
    Publisher: Royal Society of Chemistry (RSC)
    Publication Date: 2022
    detail.hit.zdb_id: 2867881-3
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  • 9
    In: Viruses, MDPI AG, Vol. 12, No. 7 ( 2020-07-17), p. 770-
    Abstract: HSV-2 (Herpes simplex virus type 2) is a critical viral agent that mainly causes genital herpes and life-long latent infection in the dorsal root ganglia. Gene modification via CRISPR/Cas9 Clustered regularly interspaced short palindromic repeat sequences/CRISPR associated 9) was used here to construct HSV-2 mutant strains through the deletion of fragments of the RL1 (Repeat Long element 1) and/or LAT (Latency-associated Transcript) genes. The HSV-2 mutant strains LAT-HSV-2 and RL1-LAT-HSV-2 present different biological properties. The proliferation of RL1-LAT-HSV-2 in nerve cells was decreased significantly, and the plaques induced by RL1-LAT-HSV-2 in Vero cells were smaller than those induced by LAT-HSV-2 mutant and wild-type strains. The observation of mice infected with these two mutants compared to mice infected with the wild-type strain indicated that the mutant RL1-LAT-HSV-2 has an attenuated phenotype with reduced pathogenicity during both acute and latent infections and induces a stronger specific immune response than the wild-type strain, whereas the attenuation effect was not found in mice infected with the LAT-HSV-2 mutant containing the LAT gene deletion. However, the simultaneous mutation of both the RL1 and LAT genes did not completely restrict viral proliferation in nerve cells, indicating that multiple HSV genes are involved in viral replication in the neural system. This work suggests that the HSV-2 genes RL1 and/or LAT might be involved in the virulence mechanisms in mouse infections.
    Type of Medium: Online Resource
    ISSN: 1999-4915
    Language: English
    Publisher: MDPI AG
    Publication Date: 2020
    detail.hit.zdb_id: 2516098-9
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  • 10
    Online Resource
    Online Resource
    Ivyspring International Publisher ; 2017
    In:  International Journal of Biological Sciences Vol. 13, No. 5 ( 2017), p. 652-659
    In: International Journal of Biological Sciences, Ivyspring International Publisher, Vol. 13, No. 5 ( 2017), p. 652-659
    Type of Medium: Online Resource
    ISSN: 1449-2288
    Language: English
    Publisher: Ivyspring International Publisher
    Publication Date: 2017
    detail.hit.zdb_id: 2179208-2
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