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  • 1
    Online Resource
    Online Resource
    Impact of Finerenone-Induced Albuminuria Reduction on Chronic Kidney Disease Outcomes in Type 2 Diabetes : A Mediation Analysis
    American College of Physicians ; 2023
    In:  Annals of Internal Medicine Vol. 176, No. 12 ( 2023-12), p. 1606-1616
    Details
    In: Annals of Internal Medicine, American College of Physicians, Vol. 176, No. 12 ( 2023-12), p. 1606-1616
    Type of Medium: Online Resource
    ISSN: 0003-4819 , 1539-3704
    URL: Article
    DOI: 10.7326/M23-1023
    RVK:
    XA 23600
    Language: English
    Publisher: American College of Physicians
    Publication Date: 2023
    detail.hit.zdb_id: 2003473-8
    detail.hit.zdb_id: 336-0
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  • 2
    Online Resource
    Online Resource
    Characteristics of genotype, drug resistance, and molecular transmission network among newly diagnosed HIV‐1 infections in Shenzhen, China
    Wiley ; 2023
    In:  Journal of Medical Virology Vol. 95, No. 7 ( 2023-07)
    Details
    In: Journal of Medical Virology, Wiley, Vol. 95, No. 7 ( 2023-07)
    Abstract: The HIV‐1 pandemic has persisted for four decades, and poses a major challenge to global public health. Shenzhen, a city with large number of migrant populations in China, is suffering HIV‐1 epidemic. It is necessary to continuously conduct the molecular surveillance among newly diagnosed HIV‐1 patients in these migrant population. In this study, plasma samples of newly diagnosed and ART‐naive HIV‐1 infections were collected from Shenzhen city in China. The partial genes of HIV‐1 gag and pol were amplified and sequenced for the analysis of genotype, drug resistance, and molecular transmission network. Ninety‐one sequences of pol gene were obtained from newly diagnosed HIV‐1 infections in Shenzhen, and seven HIV‐1 subtypes were revealed in this investigation. Among them, the circulating recombinant form (CRF) 07_BC was the mostly frequent subtype (53.8%, 49/91), followed by CRF01_AE (20.9%, 19/91), CRF55_01B (9.9%, 9/91), unique recombinant forms (URFs) (8.8%, 8/91), B (3.3%, 3/91), CRF59_01B (2.2%, 2/91), and CRF08_BC (1.1%, 1/91). The overall prevalence of pretreatment drug resistance (PDR) was 23.1% (21/91), and 52.38% (11/21) of the PDR was specific for the nonnucleotide reverse transcriptase inhibitors (NNRTIs). Furthermore, a total of 3091 pol gene sequences were used to generate 19 molecular transmission clusters, and then one growing cluster, a new cluster, and a cluster with growth reactivation were identified. The result revealed that more sexual partner, CRF_07BC subtype, and seven amino acid deletions in gag p6 region might be the influencing factors associated with the high risk of transmission behavior. Compared with CRF01_AE subtype, CRF07_BC subtype strains were more likely to form clusters in molecular transmission network. This suggests that long‐term surveillance of the HIV‐1 molecular transmission should be a critical measure to achieve a precise intervention for controlling the spread of HIV‐1 in China.
    Type of Medium: Online Resource
    ISSN: 0146-6615 , 1096-9071
    URL: Issue
    URL: Article
    DOI: 10.1002/jmv.v95.7
    DOI: 10.1002/jmv.28973
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 752392-0
    detail.hit.zdb_id: 1475090-9
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  • 3
    Online Resource
    Online Resource
    Reduced Pyrazinamidase Activity and the Natural Resistance of Mycobacterium kansasii to the Antituberculosis Drug Pyrazinamide
    American Society for Microbiology ; 1999
    In:  Antimicrobial Agents and Chemotherapy Vol. 43, No. 3 ( 1999-03), p. 537-542
    Details
    In: Antimicrobial Agents and Chemotherapy, American Society for Microbiology, Vol. 43, No. 3 ( 1999-03), p. 537-542
    Abstract: Pyrazinamide (PZA), an analog of nicotinamide, is a prodrug that requires conversion to the bactericidal compound pyrazinoic acid (POA) by the bacterial pyrazinamidase (PZase) activity of nicotinamidase to show activity against Mycobacterium tuberculosis . Mutations leading to a loss of PZase activity cause PZA resistance in M. tuberculosis. M. kansasii is naturally resistant to PZA and has reduced PZase activity along with an apparently detectable nicotinamidase activity. The role of the reduction in PZase activity in the natural PZA resistance of M. kansasii is unknown. The MICs of PZA and POA for M. kansasii were determined to be 500 and 125 μg/ml, respectively. Using [ 14 C]PZA and [ 14 C]nicotinamide, we found that M. kansasii had about 5-fold-less PZase activity and about 25-fold-less nicotinamidase activity than M. tuberculosis . The M. kansasii pncA gene was cloned on a 1.8-kb Bam HI DNA fragment, using M. avium pncA probe. Sequence analysis showed that the M. kansasii pncA gene encoded a protein with homology to its counterparts from M. tuberculosis (69.9%), M. avium (65.6%), and Escherichia coli (28.5%). Transformation of naturally PZA-resistant M. bovis BCG with M. kansasii pncA conferred partial PZA susceptibility. Transformation of M. kansasii with M. avium pncA caused functional expression of PZase and high-level susceptibility to PZA, indicating that the natural PZA resistance in M. kansasii results from a reduced PZase activity. Like M. tuberculosis , M. kansasii accumulated POA in the cells at an acidic pH; however, due to its highly active POA efflux pump, the naturally PZA-resistant species M. smegmatis did not. These findings suggest the existence of a weak POA efflux mechanism in M. kansasii .
    Type of Medium: Online Resource
    ISSN: 0066-4804 , 1098-6596
    URL: Article
    DOI: 10.1128/AAC.43.3.537
    RVK:
    XA 24552
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 1999
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    detail.hit.zdb_id: 217602-6
    SSG: 12
    SSG: 15,3
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  • 4
    Online Resource
    Online Resource
    Salicylate Reduces Susceptibility of Mycobacterium tuberculosis to Multiple Antituberculosis Drugs
    American Society for Microbiology ; 2002
    In:  Antimicrobial Agents and Chemotherapy Vol. 46, No. 8 ( 2002-08), p. 2636-2639
    Details
    In: Antimicrobial Agents and Chemotherapy, American Society for Microbiology, Vol. 46, No. 8 ( 2002-08), p. 2636-2639
    Abstract: Salicylate induces multiple antibiotic resistance in various bacterial species. Here we investigated the effect of salicylate on the susceptibility of Mycobacterium tuberculosis to a range of antituberculosis (anti-TB) drugs. In the presence of salicylate, the killing effects of isoniazid (INH), rifampin (RMP), ethambutol (EMB), streptomycin (STR), and p -aminosalicylate (PAS) were reduced, as shown with a tetrazolium redox dye viability assay and a bacterial survival assay. Salicylate-induced resistance was more pronounced for PAS, STR, and EMB but was not apparent for INH and RMP when salicylate and the anti-TB agents were incorporated into 7H11 plates. The significance of these findings for TB treatment needs to be further evaluated in vivo.
    Type of Medium: Online Resource
    ISSN: 0066-4804 , 1098-6596
    URL: Article
    DOI: 10.1128/AAC.46.8.2636-2639.2002
    RVK:
    XA 24552
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2002
    detail.hit.zdb_id: 1496156-8
    detail.hit.zdb_id: 217602-6
    SSG: 12
    SSG: 15,3
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  • 5
    Online Resource
    Online Resource
    Abstract 4873: IKKα bridges central tolerance to innate immunity and inflammation
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 19_Supplement ( 2014-10-01), p. 4873-4873
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. 4873-4873
    Abstract: IKKα has emerged as a tumor suppressor in squamous cell carcinomas (SCCs) of skin, head and neck, and lung. Our recent studies indicate that inflammation is involved in lung SCCs in kinase-dead knock-in IkkαKA/KA mice. However, how IKKα prevents inflammation has not been fully understood yet. In the present studies, we showed that IkkαKA/KA mice developed reduced thymic medullary regions, systemic inflammation, and severe skin damage, indicating that IKKα plays an essential role linking central tolerance to innate immunity and inflammation. In line with previous studies of the role of NF-κB pathway in thymic medulla formation and the establishment of central tolerance, we found that NF-κB pathway was inactivated in the presence of kinase inactive form of IKKα in thymic epithelial cells. Depleting the lymphocytes, thymus, T cells, macrophages, and/or reintroducing transgenic IKKα into the skin or thymus rescued the severe skin phenotypes. Transferring IkkαKA/KA T cells, but not wild-type T cells, reconstituted the severe skin phenotypes and SCCs in the lungs and forestomach of IkkαKA/KA/Rag-/- mice. We found that the self-reactive T cells provided TGFβ signaling, which enhanced the expression of monocyte chemoattractant protein-1 (MCP-1) in keratinocytes. As a result, increased level of MCP-1 led to robust recruitment of macrophages to the skin, resulting in skin inflammation and hyperproliferation. This study reveals an important IKKα/TGFβ/MCP-1 signaling axis that orchestrates central tolerance and inflammation in the maintenance of tissue homeostasis. Citation Format: Feng Zhu, Zhisong Chen, Jami Willette-Brown, Dakshayani Lomada, Sean R. Davis, Timothy Back, Teizo Yoshimura, Zhonghe Sun, Xiaolin Wu, Robert Wiltrout, Ellen Richie, Ulrich Siebenlist, Giorgio Trichieri, Yinling Hu. IKKα bridges central tolerance to innate immunity and inflammation. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4873. doi:10.1158/1538-7445.AM2014-4873
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2014-4873
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
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  • 6
    Online Resource
    Online Resource
    Abstract 1083: The pivotal role of IKKalpha in the development of spontaneous lung squamous cell carcinomas.
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 8_Supplement ( 2013-04-15), p. 1083-1083
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 8_Supplement ( 2013-04-15), p. 1083-1083
    Abstract: During the last decades lung cancer has become the leading cause of cancer deaths in the world, and the need to develop better diagnostic techniques and therapies is urgent. To advance the understanding of this disease, various genetically engineered and chemical induced mouse models have been established. However, there are no robust animal models of lung squamous cell carcinomas (SCCs), one of the major types of lung cancer. Here, we generated Ikkα-KA/KA knock-in mice (KA/KA) in which an ATP binding site of IKKα, Lys 44 was replaced by alanine. All the knock-in mice at 4 to 6 months of age developed spontaneous lethal lung SCCs associated with markedly increased leukocyte infiltration and expression of cytokines, and chemokines in the lungs. Furthermore, we identified deregulated c-myc, Nanog, Oct3/4, p53, Rb, EGFR, MAPK, Jun-B, p63, Trim29, Rhov, CDK1, and IGF1 in mouse lung SCCs, and identified reduced IKKα and IκBα and increased ROS1 in mutant lungs and SCCs, some of which were found in human lung SCCs. Lung cancers were prevented by reintroducing epithelial-cell IKKα, depleting macrophages or depleting lymphocytes. This study not only provides a novel model for studying the pathogenesis, treatment, early detection, and prevention of human lung SCCs, but also demonstrates how a single mutation in IKKα elicits malignancy through the combined epithelial-cell-autonomous and immune mechanisms. Citation Format: Zuoxiang Xiao, Qun Jiang, Jami Willette-Brown, Feng Zhu, Sichuan Xi, Sandra Burkett, Fanching Lin, Timothy Back, Mahesh Datla, Zhonghe Sun, Romina Goldszmid, Xiaolin Wu, David Schrump, Howard Young, Georgio Trinchieri, Robert Wiltrout, Yinling Hu. The pivotal role of IKKalpha in the development of spontaneous lung squamous cell carcinomas. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1083. doi:10.1158/1538-7445.AM2013-1083
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2013-1083
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
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  • 7
    Online Resource
    Online Resource
    Conditions that may affect the results of susceptibility testing of Mycobacterium tuberculosis to pyrazinamide
    Microbiology Society ; 2002
    In:  Journal of Medical Microbiology Vol. 51, No. 1 ( 2002-01-01), p. 42-49
    Details
    In: Journal of Medical Microbiology, Microbiology Society, Vol. 51, No. 1 ( 2002-01-01), p. 42-49
    Type of Medium: Online Resource
    ISSN: 0022-2615 , 1473-5644
    URL: Article
    DOI: 10.1099/0022-1317-51-1-42
    RVK:
    XA 55020
    Language: English
    Publisher: Microbiology Society
    Publication Date: 2002
    detail.hit.zdb_id: 2083944-3
    detail.hit.zdb_id: 218356-0
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    An Imprinted Locus Epistatically Influences Nstr1 and Nstr2 to Control Resistance to Nerve Sheath Tumors in a Neurofibromatosis Type 1 Mouse Model
    American Association for Cancer Research (AACR) ; 2006
    In:  Cancer Research Vol. 66, No. 1 ( 2006-01-01), p. 62-68
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 66, No. 1 ( 2006-01-01), p. 62-68
    Abstract: Cancer is a complex disease in which cells acquire many genetic and epigenetic alterations. We have examined how three types of alterations, mutations in tumor suppressor genes, changes in an imprinted locus, and polymorphic loci, interact to affect tumor susceptibility in a mouse model of neurofibromatosis type 1 (NF1). Mutations in tumor suppressor genes such as TP53 and in oncogenes such as KRAS have major effects on tumorigenesis due to the central roles of these genes in cell proliferation and cell survival. Imprinted genes expressed from only one parental chromosome affect tumorigenesis if their monoallelic expression is lost or duplicated. Because imprinted loci are within regions deleted or amplified in cancer, the parental origin of genomic rearrangements could affect tumorigenesis. Gene polymorphisms can vary tumor incidence by affecting rate-limiting steps in tumorigenesis within tumor cells or surrounding stroma. In our mouse model of NF1, the incidence of tumors mutant for the tumor suppressor genes Nf1 and Trp53 is strongly modified by a linked imprinted locus acting epistatically on two unlinked polymorphic loci, Nstr1 and Nstr2. This interaction of an imprinted locus and polymorphic susceptibility loci has profound implications for human mapping studies where the parental contribution of alleles is often unknown. (Cancer Res 2006; 66(1): 62-8)
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-05-1480
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2006
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
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