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  • Medicine  (65)
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  • 1
    Online Resource
    Online Resource
    Single-cell analyses and host genetics highlight the role of innate immune cells in COVID-19 severity
    Springer Science and Business Media LLC ; 2023
    In:  Nature Genetics Vol. 55, No. 5 ( 2023-05), p. 753-767
    Details
    In: Nature Genetics, Springer Science and Business Media LLC, Vol. 55, No. 5 ( 2023-05), p. 753-767
    Abstract: Mechanisms underpinning the dysfunctional immune response in severe acute respiratory syndrome coronavirus 2 infection are elusive. We analyzed single-cell transcriptomes and T and B cell receptors (BCR) of 〉 895,000 peripheral blood mononuclear cells from 73 coronavirus disease 2019 (COVID-19) patients and 75 healthy controls of Japanese ancestry with host genetic data. COVID-19 patients showed a low fraction of nonclassical monocytes (ncMono). We report downregulated cell transitions from classical monocytes to ncMono in COVID-19 with reduced CXCL10 expression in ncMono in severe disease. Cell–cell communication analysis inferred decreased cellular interactions involving ncMono in severe COVID-19. Clonal expansions of BCR were evident in the plasmablasts of patients. Putative disease genes identified by COVID-19 genome-wide association study showed cell type-specific expressions in monocytes and dendritic cells. A COVID-19-associated risk variant at the IFNAR2 locus (rs13050728) had context-specific and monocyte-specific expression quantitative trait loci effects. Our study highlights biological and host genetic involvement of innate immune cells in COVID-19 severity.
    Type of Medium: Online Resource
    ISSN: 1061-4036 , 1546-1718
    URL: Article
    DOI: 10.1038/s41588-023-01375-1
    RVK:
    XA 10000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 1494946-5
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    CRTH2 Is A Critical Regulator of Neutrophil Migration and Resistance to Polymicrobial Sepsis
    The American Association of Immunologists ; 2012
    In:  The Journal of Immunology Vol. 188, No. 11 ( 2012-06-01), p. 5655-5664
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 188, No. 11 ( 2012-06-01), p. 5655-5664
    Abstract: Although arachidonic acid cascade has been shown to be involved in sepsis, little is known about the role of PGD2 and its newly found receptor, chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTH2), on the septic response. Severe sepsis is associated with the failure of neutrophil migration. To investigate whether CRTH2 influences neutrophil recruitment and the lethality during sepsis, sepsis was induced by cecal ligation and puncture (CLP) surgery in mice. CRTH2 knockout (CRTH2−/−) mice were highly resistant to CLP-induced sepsis, which was associated with lower bacterial load and lower production of TNF-α, IL-6, and CCL3. IL-10, an anti-inflammatory cytokine, was higher in CRTH2−/− mice, blunting CLP-induced lethality in CRTH2−/− mice. Neutrophil accumulation in the peritoneum was more pronounced after CLP in CRTH2−/− mice, which was associated with higher CXCR2 levels in circulating neutrophils. Furthermore, sepsis caused a decrease in the level of acetylation of histone H3, an activation mark, at the CXCR2 promoter in wild-type neutrophils, suggesting that CXCR2 expression levels are epigenetically regulated. Finally, both pharmacological depletion of neutrophils and inhibition of CXCR2 abrogated the survival benefit in CRTH2−/− mice. These results demonstrate that genetic ablation of CRTH2 improved impaired neutrophil migration and survival during severe sepsis, which was mechanistically associated with epigenetic-mediated CXCR2 expression. Thus, CRTH2 is a potential therapeutic target for polymicrobial sepsis.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1102330
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2012
    detail.hit.zdb_id: 1475085-5
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  • 3
    Online Resource
    Online Resource
    Inhibition of c-Jun NH2-Terminal Kinase Activity Improves Ischemia/Reperfusion Injury in Rat Lungs
    The American Association of Immunologists ; 2004
    In:  The Journal of Immunology Vol. 172, No. 4 ( 2004-02-15), p. 2569-2577
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 172, No. 4 ( 2004-02-15), p. 2569-2577
    Abstract: Although c-Jun NH2-terminal kinase (JNK) has been implicated in the pathogenesis of transplantation-induced ischemia/reperfusion (I/R) injury in various organs, its significance in lung transplantation has not been conclusively elucidated. We therefore attempted to measure the transitional changes in JNK and AP-1 activities in I/R-injured lungs. Subsequently, we assessed the effects of JNK inhibition by the three agents including SP600125 on the degree of lung injury assessed by means of various biological markers in bronchoalveolar lavage fluid and histological examination including detection of apoptosis. In addition, we evaluated the changes in p38, extracellular signal-regulated kinase, and NF-κB-DNA binding activity. I/R injury was established in the isolated rat lung preserved in modified Euro-Collins solution at 4°C for 4 h followed by reperfusion at 37°C for 3 h. We found that AP-1 was transiently activated during ischemia but showed sustained activation during reperfusion, leading to significant lung injury and apoptosis. The change in AP-1 was generally in parallel with that of JNK, which was activated in epithelial cells (bronchial and alveolar), alveolar macrophages, and smooth muscle cells (bronchial and vascular) on immunohistochemical examination. The change in NF-κB qualitatively differed from that of AP-1. Protein leakage, release of lactate dehydrogenase and TNF-α into bronchoalveolar lavage fluid, and lung injury were improved, and apoptosis was suppressed by JNK inhibition. In conclusion, JNK plays a pivotal role in mediating lung injury caused by I/R. Therefore, inhibition of JNK activity has potential as an effective therapeutic strategy for preventing I/R injury during lung transplantation.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.172.4.2569
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2004
    detail.hit.zdb_id: 1475085-5
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  • 4
    Online Resource
    Online Resource
    Effect of inflammation-associated cytokines of biliary tract cancer on chemoresistance and therapeutic implications.
    American Society of Clinical Oncology (ASCO) ; 2014
    In:  Journal of Clinical Oncology Vol. 32, No. 3_suppl ( 2014-01-20), p. 247-247
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 32, No. 3_suppl ( 2014-01-20), p. 247-247
    Abstract: 247 Background: Biliary tract cancer (BTC) is well-known to be commonly suffered from inflammations; cholangitis and/or liver abscess. The author previously showed interleukin-6 (IL-6) worked on anti-apoptotic process in BTC. Herein, we focused on inflammation-associated cytokines including not only IL-6 but also transforming growth factor-beta 1 (TGF-β1), and investigated the working processes, their relationship to chemoresistance, and therapeutic implications. Methods: We employed resected specimens and BTC cell lines. We evaluated IL-6/TGF-β1 expression, invasion, endothelial-mesenchymal transition (EMT), and chemoresistance to gemcitabine, with or without silencing of PI3K/Akt, MAPK, STAT, and Smad pathways. Results: Resected specimens expressed IL6 and TGF-β1 staining at the invasion front by immunohistochemical staining. In BTC cell lines, spontaneous expression of IL-6/TGF-β1 was related to malignant potencies such as EMT and chemoresistance. Rh IL-6/TGF-β1 induced invasion, EMT, and chemoresistance. Smad4 among cell signaling pathways functioned in a dominant manner; inhibition of Smad4 pathway reduced invasion, and reversed EMT and chemoresistance, in both rh IL-6/TGF-β1-treated cells, and we confirmed these results using SMAD4 siRNA. And, our established gemcitabine-resistant cells expressed high level of IL-6/TGF-β1, and promoted EMT. Inhibition of Smad4 also reversed chemoresistance in gemcitabine-resistant cells. We confirmed N-cadherin and Smad4 expression at the invasion front by immunohistochemistry. Conclusions: IL-6 and TGF-β1 resulted in chemoresistance, and inhibition of Smad4 would reverse chemoresistance in BTC.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2014.32.3_suppl.247
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2014
    detail.hit.zdb_id: 2005181-5
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  • 5
    Online Resource
    Online Resource
    Assessment of PD-L1 expression and oncogenic gene status in patients with small-cell lung cancer: Immuno-oncology biomarker study in LC-SCRUM-Japan.
    American Society of Clinical Oncology (ASCO) ; 2019
    In:  Journal of Clinical Oncology Vol. 37, No. 15_suppl ( 2019-05-20), p. 8558-8558
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 37, No. 15_suppl ( 2019-05-20), p. 8558-8558
    Abstract: 8558 Background: The clinical impact of PD-L1 expression and oncogenic gene status in patients with small cell lung cancer (SCLC) is not well characterized. We initiated this immuno-oncology biomarker study as part of nationwide genomic screening by LC-SCRUM-Japan (LC-SCRUM-IBIS). Methods: Tumor samples from lung cancer patients enrolled in LC-SCRUM-IBIS were primarily subjected to targeted next-generation sequencing (NGS) with Oncomine™ Comprehensive Assay. The PD-L1 expression was also analyzed by 4 immunohistochemistry (IHC) assays for 22C3, 28-8, SP263 and SP142. At this analysis, 22C3, 28-8, and SP263 were assessed in tumor cells (TC) as positive in 〉 1%, and SP142 in both TC and tumor-infiltrating immune cells (IC) as positive in 〉 TC1/IC1, as previously reported. The association of PD-L1 expression, oncogenic gene status and clinical outcome was investigated in SCLC patients. Results: Between Feb 2017 and May 2018, 1017 lung cancer patients were enrolled in LC-SCRUM-IBIS. Among them, 933 patients had adequate tumor samples including 101 SCLC and 832 non-small cell lung cancer. Of 101 SCLC patients, the results of PD-L1 expression by 4 IHC assays were 18% in 22C3, 17% in 28-8, 11% in SP263 and 8% in SP142, respectively. Targeted NGS showed that 8 patients had at least one targetable oncogenic alterations, including 3 PIK3CA and 1 KRAS as mutations and 3 PTEN and 1 TSC2 as inactivating mutations. PD-L1 expression by 22C3 was associated with good performance status (P = 0.05) and the presence of oncogenic alterations (P = 0.004). PD-L1 status was not associated with response to cytotoxic chemotherapy and progression-free survival and overall survival in first-line treatment of SCLC patients. Conclusions: The frequency of PD-L1 expression in SCLC patients was relatively lower compared with that reported in other solid tumors. PD-L1 status by TC in 22C3 appears to be not correlated with clinical outcomes for cytotoxic chemotherapy of SCLC patients. Further investigation is needed to explore a predictive biomarker for immune checkpoint inhibitors. Updated results will be presented at the meeting.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.2019.37.15_suppl.8558
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2019
    detail.hit.zdb_id: 2005181-5
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  • 6
    Online Resource
    Online Resource
    The referential survival data of borderline resectable pancreatic cancer (BRPC) patients who are candidate for neoajuvant chemotherapy followed by surgery.
    American Society of Clinical Oncology (ASCO) ; 2015
    In:  Journal of Clinical Oncology Vol. 33, No. 3_suppl ( 2015-01-20), p. 434-434
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 33, No. 3_suppl ( 2015-01-20), p. 434-434
    Abstract: 434 Background: The aim of this study is to clarify referential survival data of BRPC patients who are candidate for neoajuvant chemotherapy followed by surgery. Methods: This retrospective study included data from all consecutive patients who were diagnosed as having invasive ductal pancreatic cancer at our hospital between January 2008 and December 2013. Selection criteria were as follows: patients who 1) had histologically confirmed pancreatic adenocarcinoma, 2) were diagnosed as having non-metastatic disease by dynamic CT before treatment, 3) had received anti-cancer treatment, and had been observed for 3 months or longer. We reviewed CT stage (UICC) and treatment modality, and analyzed their survival data. Results: There were 428 patients who met the selection criteria. Among them, clinical CT stage I/II (Group A; potentially respectable) and stage III (Group B; locally advanced) were documented in 170 (40%) and 131, respectively. Laparotomy was performed in all patients in Group A. Of the 170 in Group A, 166 (98%) received resection with curative intent, and the remaining 4 did not received resection because of discovery of occult metastasis at laparotomy. Of the 131 in Group B, 36 (27%; Group B-1) received resection with curative intent, 7 did not received resection because of occult metastasis, and the remaining 88 did not receive laparotomy because they were diagnosed as having locally advanced unresectable disease by CT. Among Group B, patients other than Group B-1 received gemcitabine-based chemotherapy (Group B-2; N=95). The median survival time, 1-yr, 2-yr, and 3-yr survival rate were 28.7 months, 78.6%, 55.5%, and 38.9% in Group A, 16.8 months, 63.8%, 31.8%, and 19.8% in Group B-1, and 13.8 months, 60.1%, 21.7%, and 5.9% in Group B-2, respectively. Conclusions: Based on our historical data, we suppose that 16.8 months of median survival time or survival rate of 19.8 at 3-yr, i.e, Group B-1 survival data, may be an appropriate threshold value in the single-arm phase 2 BRPC study.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2015.33.3_suppl.434
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2015
    detail.hit.zdb_id: 2005181-5
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  • 7
    Online Resource
    Online Resource
    A retrospective study of FOLFOX in the treatment of patients with advanced duodenal adenocarcinoma: A Japanese single-center experience.
    American Society of Clinical Oncology (ASCO) ; 2015
    In:  Journal of Clinical Oncology Vol. 33, No. 3_suppl ( 2015-01-20), p. 457-457
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 33, No. 3_suppl ( 2015-01-20), p. 457-457
    Abstract: 457 Background: Duodenal adenocarcinoma is a rare tumor with poor prognosis. There is little data on the efficacy of chemotherapy for this disease. Methods: The current study included data from all consecutive patients who were diagnosed as having duodenal adenocarcinoma at our hospital between October 2008 and December 2013. Selection criteria were as follows: patients who 1) had histologically confirmed duodenal adenocarcinoma, 2) were diagnosed as having unresectable or recurrent disease, and 3) received first-line chemotherapy with infusional 5-FU, leucovorin and oxaliplatin (FOLFOX). We examined efficacy and toxicity of FOLFOX therapy from the case cards and analyzed their survival data. Results: There were 20 patients who met the selection criteria. The median age was 67.5 years (range, 35-76). Of the 20, 11 (45%) were male, 17 (85%) had a good performance status, 15 (75%) had received resection of the primary tumor, and 13 (65%) had a liver metastasis. They received median of 8 (range, 1-32) chemotherapy cycles. There was no complete response. Of the 20, 4 (20%) achieved partial response, 9 (45%) remained stable disease, 6 (30%) showed progressive disease and the remaining one did not have a CT evaluation. The median progression free survival and overall survival months from the initiation of FOLFOX therapy were 5.0 and 11.7, respectively. Grade 3/4 toxicities were observed in 9 (45%). Although there was no febrile neutropenia, grade 3/4 neutropenia was observed in 7 (35%). Treatment-related death due to pneumonitis was documented in one. Whereas prognostic factor was not found in multivariate analysis, a peritoneum metastasis tended to be associated with poor progression free survival (p=0.06). Conclusions: The FOLFOX therapy shows moderately activity with acceptable toxicities for the treatment of advanced duodenal adenocarcinoma.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2015.33.3_suppl.457
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2015
    detail.hit.zdb_id: 2005181-5
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  • 8
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    Online Resource
    Reconsidering the cutoff between sensitive and refractory relapses in extensive-stage small cell lung cancer in the era of immunotherapy.
    American Society of Clinical Oncology (ASCO) ; 2023
    In:  Journal of Clinical Oncology Vol. 41, No. 16_suppl ( 2023-06-01), p. 8576-8576
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 41, No. 16_suppl ( 2023-06-01), p. 8576-8576
    Abstract: 8576 Background: The use of platinum-based doublet chemotherapy combined with immune checkpoint inhibitors (ICIs) has demonstrated promising outcomes in the first-line treatment of extensive-stage small cell lung cancer (ES-SCLC). Relapsed SCLC has been classified into "sensitive" or "refractory" relapse types according to cutoff values (60 or 90 days) of duration from the last chemotherapy administration to disease progression. However, it is unclear whether these cutoff values can be applied to ICI combination therapy. Methods: We retrospectively analyzed a multicenter database of ES-SCLC patients who received second-line therapy after the platinum-etoposide plus ICI (atezolizumab or durvalumab). An optimal cutoff value for the platinum-free interval (PFI) was selected, which minimized the two-sided p-value and maximized hazard ratio (HR) regarding relapse type (sensitive or refractory according to a cutoff value) calculated from a multivariable Cox regression model for overall survival (OS) including performance status (PS) and sex as covariates. The internal validity of the selected cutoff value was assessed via two-fold cross-validation (CV) manner. Results: A total of 101 patients (61 deaths) from 10 hospitals were included in the study. The median follow-up period was 21.1 months. The optimal cutoff value was 75 days (p=0.0002), and when applying this cutoff value, median OS was 15.9 and 5.0 months of sensitive- (n=51) and refractory- (n=50) relapsed patients, and the HR calculated from a two-fold CV was 3.13 (95% confidence interval [CI], 1.66 to 5.90). Additionally, traditional cutoff values of 60 and 90 days also predicted prognosis better, but cutoff values of 110 days or longer did not (Table). Conclusions: Even in the era of combined immunotherapy in ES-SCLC patients, the threshold days for classifying as sensitive- or refractory- relapse did not exhibit a significant change compared to the pre-immunotherapy era. Although further validation studies with a larger sample size would be needed, relapse type classification using the selected cutoff value of 75 days is worth considering as a new prognostic factor for relapsed ES-SCLC patients. [Table: see text]
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.2023.41.16_suppl.8576
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2023
    detail.hit.zdb_id: 2005181-5
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  • 9
    Online Resource
    Online Resource
    Targeting a Complex Transcriptome: The Construction of the Mouse Full-Length cDNA Encyclopedia
    Cold Spring Harbor Laboratory ; 2003
    In:  Genome Research Vol. 13, No. 6b ( 2003-06), p. 1273-1289
    Details
    In: Genome Research, Cold Spring Harbor Laboratory, Vol. 13, No. 6b ( 2003-06), p. 1273-1289
    Abstract: We report the construction of the mouse full-length cDNA encyclopedia,the most extensive view of a complex transcriptome,on the basis of preparing and sequencing 246 libraries. Before cloning,cDNAs were enriched in full-length by Cap-Trapper,and in most cases,aggressively subtracted/normalized. We have produced 1,442,236 successful 3′-end sequences clustered into 171,144 groups, from which 60,770 clones were fully sequenced cDNAs annotated in the FANTOM-2 annotation. We have also produced 547,149 5′ end reads,which clustered into 124,258 groups. Altogether, these cDNAs were further grouped in 70,000 transcriptional units (TU),which represent the best coverage of a transcriptome so far. By monitoring the extent of normalization/subtraction, we define the tentative equivalent coverage (TEC),which was estimated to be equivalent to 〉 12,000,000 ESTs derived from standard libraries. High coverage explains discrepancies between the very large numbers of clusters (and TUs) of this project,which also include non-protein-coding RNAs,and the lower gene number estimation of genome annotations. Altogether,5′-end clusters identify regions that are potential promoters for 8637 known genes and 5′-end clusters suggest the presence of almost 63,000 transcriptional starting points. An estimate of the frequency of polyadenylation signals suggests that at least half of the singletons in the EST set represent real mRNAs. Clones accounting for about half of the predicted TUs await further sequencing. The continued high-discovery rate suggests that the task of transcriptome discovery is not yet complete.
    Type of Medium: Online Resource
    ISSN: 1088-9051
    URL: Article
    DOI: 10.1101/gr.1119703
    RVK:
    XA 10000
    Language: English
    Publisher: Cold Spring Harbor Laboratory
    Publication Date: 2003
    detail.hit.zdb_id: 1483456-X
    SSG: 12
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  • 10
    Online Resource
    Online Resource
    Perampanel for Sporadic Amyotrophic Lateral Sclerosis (138)
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Neurology Vol. 94, No. 15_supplement ( 2020-04-14)
    Details
    In: Neurology, Ovid Technologies (Wolters Kluwer Health), Vol. 94, No. 15_supplement ( 2020-04-14)
    Type of Medium: Online Resource
    ISSN: 0028-3878 , 1526-632X
    URL: Article
    DOI: 10.1212/WNL.94.15_supplement.138
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
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