X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Online Resource
    Online Resource
    The cultivation of human multipotent mesenchymal stromal cells in clinical grade medium for bone tissue engineering
    Elsevier BV ; 2009
    In:  Biomaterials Vol. 30, No. 20 ( 2009-07), p. 3415-3427
    Details
    In: Biomaterials, Elsevier BV, Vol. 30, No. 20 ( 2009-07), p. 3415-3427
    Type of Medium: Online Resource
    ISSN: 0142-9612
    URL: Article
    DOI: 10.1016/j.biomaterials.2009.03.001
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2009
    detail.hit.zdb_id: 2004010-6
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 2
    Online Resource
    Online Resource
    MCL1 Targeting Agent Homoharringtonine Exerts Strong Cytotoxicity Towards Diffuse Large B-Cell Lymphoma (DLBCL) Cells and Synergizes with BCL2 Targeting Agent ABT199 in Eliminating BCL2-Positive DLBCL Cells
    American Society of Hematology ; 2014
    In:  Blood Vol. 124, No. 21 ( 2014-12-06), p. 3645-3645
    Details
    In: Blood, American Society of Hematology, Vol. 124, No. 21 ( 2014-12-06), p. 3645-3645
    Abstract: Introduction: Diffuse large B-cell lymphoma (DLBCL) represents the most prevalent type of B-cell non-Hodgkin lymphomas (B-NHL) in the Western hemisphere. While BCL2 gene deregulation was repeatedly associated with poor prognosis, the role of MCL1 in the biology of DLBCL remains largely unknown. ABT199 is a highly-selective inhibitor of BCL2 protein currently evaluated in clinical trials. Homoharringtonine (HHT) is a plant alkaloid and as a semisynthetic compound (omacetaxine) it was approved for the treatment of relapsed chronic myelogenous leukemia (CML). Anti-tumor activity of HHT includes downregulation of the anti-apoptotic protein MCL1. Aim: The aim of the project was to evaluate the preclinical anti-lymphoma efficacy of BCL2 and MCL1-targeting agents ABT199 and HHT in DLBCL. Methods: Immunophenotype of primary DLBCL samples was determined by immunohistochemistry (IHC) using the Hans algorithm. Sensitivity of DLBCL cell lines to ABT199 and HHT was determined by Annexin V-based apoptotic assay and WST8-based cell proliferation assay. DLBCL clones with downregulation of selected anti-apoptotic proteins were derived using pLKO1-based lentiviral particles containing shRNAs against BCL2, BCL-XL and MCL1. For upregulation, BCL2, BCL-XL and MCL1 were cloned in the lentiviral expression vector pCDHNeo and the prepared lentiviral particles were used for the transduction of DLBCL cell lines. Results: We analyzed molecular mechanisms of cytotoxic activity of HHT in 7 DLBCL cell lines, and confirmed decreased expression of MCL1 protein in all cases. By semi-quantitative protein expression analysis (western blot or IHC) we demonstrated that BCL-XL and MCL1 were detectable in all DLBCL cell lines (n=18) and primary samples (n=114, GCB=51, ABC=63), while BCL2 was not detectable in 6 out of 18 DLBCL cell lines and 32 out of 114 primary DLBCL samples. 8 out of 12 BCL2-positive DLBCL cell lines were sensitive to 1 microM ABT199 (i.e. did not survive 1 microM ABT199 by standard proliferation assay). In contrary, 6 out of 6 BCL2-negative DLBCL cell lines were resistant to 1 microM ABT199. 11 out of 12 BCL2-positive DLBCL cell lines were sensitive to 30 nM HHT (considered a steady-state plasma level in CML patients treated with HHT). 5 out of 6 BCL2-negative DLBCL cell lines were sensitive to 30 nM HHT. Significant drug synergism between ≤1 microM ABT199 and ≤ 30 nM HHT was observed in 8 out of 12 BCL2-positive, but only in 1 out of 6 BCL2-negative DLBCL cell lines. We demonstrated that high expression of BCL2 positively correlated with sensitivity to ABT-199, irrespective of expression levels of BCL-XL and MCL1. Expression levels of BCL2 and BCL-XL negatively correlated with sensitivity to HHT. Expression level of MCL1 did not correlate with sensitivity to HHT. Both targeted downregulation and transgenic overexpression of BCL-XL in selected DLBCL cell lines confirmed that the expression of BCL-XL negatively correlates with sensitivity to HHT (but not to ABT199). While increase in sensitivity to HHT was observed in 3 out of 3 DLBCL cell lines with targeted knock-down of BCL2, increase in sensitivity to ABT199 was observed only in 1 out of these 3 DLBCL cell lines. Targeted knockdown of MCL1 was associated with increased sensitivity to HHT in 1 out of 2 DLBCL cell lines, but with no change of sensitivity to ABT199. Conclusions: HHT is a promising anti-DLBCL agent in both BCL2-positive and BCL2-negative cases. ABT199, as a single-agent or in combination with HHT, effectively eliminates BCL2-positive DLBCL cells. Based on the observed data two biological categories of DLBCL might be assumed: BCL2-dependent (ABT199-sensitive, HHT-sensitive) and MCL1-dependent (ABT199-resistant, HHT-sensitive) DLBCL. Grant support: IGA-MZ: NT13201-4/2012, GACR14-19590S, UNCE 204021, SVV-2013-266509, PRVOUK P24/LF1/3, GA-UK 1270214 Disclosures No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V124.21.3645.3645
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2014
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 3
    Online Resource
    Online Resource
    Targeting of BCL2 Family Proteins with ABT-199 and Homoharringtonine Reveals BCL2- and MCL1-Dependent Subgroups of Diffuse Large B-Cell Lymphoma
    American Association for Cancer Research (AACR) ; 2016
    In:  Clinical Cancer Research Vol. 22, No. 5 ( 2016-03-01), p. 1138-1149
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 22, No. 5 ( 2016-03-01), p. 1138-1149
    Abstract: Purpose: To investigate the roles of BCL2, MCL1, and BCL-XL in the survival of diffuse large B-cell lymphoma (DLBCL). Experimental designs: Immunohistochemical analysis of 105 primary DLBCL samples, and Western blot analysis of 18 DLBCL cell lines for the expression of BCL2, MCL1, and BCL-XL. Pharmacologic targeting of BCL2, MCL1, and BCL-XL with ABT-199, homoharringtonine (HHT), and ABT-737. Analysis of DLBCL clones with manipulated expressions of BCL2, MCL1, and BCL-XL. Immunoprecipitation of MCL1 complexes in selected DLBCL cell lines. Experimental therapy aimed at inhibition of BCL2 and MCL1 using ABT-199 and HHT, single agent, or in combination, in vitro and in vivo on primary cell-based murine xenograft models of DLBCL. Results: By the pharmacologic targeting of BCL2, MCL1, and BCL-XL, we demonstrated that DLBCL can be divided into BCL2-dependent and MCL1-dependent subgroups with a less pronounced role left for BCL-XL. Derived DLBCL clones with manipulated expressions of BCL2, MCL1, and BCL-XL, as well as the immunoprecipitation experiments, which analyzed MCL1 protein complexes, confirmed these findings at the molecular level. We demonstrated that concurrent inhibition of BCL2 and MCL1 with ABT-199 and HHT induced significant synthetic lethality in most BCL2-expressing DLBCL cell lines. The marked cytotoxic synergy between ABT-199 and HHT was also confirmed in vivo using primary cell-based murine xenograft models of DLBCL. Conclusions: As homoharringtonine is a clinically approved antileukemia drug, and ABT-199 is in advanced phases of diverse clinical trials, our data might have direct implications for novel concepts of early clinical trials in patients with aggressive DLBCL. Clin Cancer Res; 22(5); 1138–49. ©2015 AACR.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-15-1191
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2016
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 4
    Online Resource
    Online Resource
    Retrospective analysis of 235 unselected patients with mantle cell lymphoma confirms prognostic relevance of Mantle Cell Lymphoma International Prognostic Index and Ki-67 in the era of rituximab: long-term data from the Czech Lymphoma Project Database
    Informa UK Limited ; 2014
    In:  Leukemia & Lymphoma Vol. 55, No. 4 ( 2014-04), p. 802-810
    Details
    In: Leukemia & Lymphoma, Informa UK Limited, Vol. 55, No. 4 ( 2014-04), p. 802-810
    Type of Medium: Online Resource
    ISSN: 1042-8194 , 1029-2403
    URL: Article
    DOI: 10.3109/10428194.2013.815349
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 2014
    detail.hit.zdb_id: 2030637-4
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 5
    Online Resource
    Online Resource
    Upregulation of Caspase 10 Contributes to Acquired Resistance of Acute T-Lymphoblastic Leukemia Cells to Proapoptotic Cytokine TRAIL.
    American Society of Hematology ; 2009
    In:  Blood Vol. 114, No. 22 ( 2009-11-20), p. 3790-3790
    Details
    In: Blood, American Society of Hematology, Vol. 114, No. 22 ( 2009-11-20), p. 3790-3790
    Abstract: Abstract 3790 Poster Board III-726 TNF-related apoptosis inducing ligand (TRAIL) is a death ligand with selective antitumor activity and minimal cytotoxicity toward non-malignant tissues. TRAIL is under evaluation in several clinical trials in the treatment of diverse cancers, including hematologic malignancies. Molecular mechanisms responsible for acquired TRAIL resistance (e.g. following treatment with TRAIL) are largely unknown. TRAIL-sensitive T-lymphoblastic leukemia cell line Jurkat was cultivated for 8 weeks with TRAIL (1mg/mL). Three TRAIL-resistant Jurkat subclones (TR1-3) were derived and subjected to analysis. Acquired TRAIL-resistance was asociated with decreased sensitivity to several of the tested cytotoxic agents (including TNF-alpha, Fas-ligand, fludarabine and methotrexate), while sensitivity to other agents was unchanged (doxorubicin, cisplatin, etoposid) or even increased (cytarabine). TRAIL-resistant subclones did not show significant differences either in the cell surface expression of death ligand receptors (TRAIL-R1-4, TNF-R, Fas) or in the protein levels of key antiapoptotic regulators (e.g. Bcl2, Mcl1, XIAP, Survivin). Surprisingly, the most prominent finding was significant upregulation of apical proapoptotic caspase 10 (CASP10) in subclone TR1 on mRNA (3-fold increase) as well as on protein level. Moreover, downregulation of CASP8 was detected in subclone TR1 both by western blotting and real-time RT-PCR. siRNA-induced inhibition of protein CASP10 in subclone TR1 was associated with partial restoration of sensitivity to TRAIL-induced apoptosis. No relevant mutations were revealed by sequencing of CASP10 transcript variants A and D of TR1 subclone compared to TRAIL-sensitive Jurkat cells. Immunoprecipitation (IP) analysis of death-inducing signaling complex (DISC) using biotinylated TRAIL suggested impaired DICS formation in subclones TR2 and TR3, but not in TR1. DISC analysis also demonstrated that CASP10 was physically bound in the DISC of TR1 subclone after exposure to TRAIL. Preincubation of the TR subclones with several histone-deacetylase inhibitors (HDACi: vorinostat, sodium valproate or sodium butyrate) for 12 hours almost completely restored sensitivity to TRAIL. Immunoprecipitation analysis of DISC showed treatment with HDACi for 12h resulted in substantially increased binding of precleaved CASP8 (55kD and 43kD) and precleaved CASP10 (53kD) to the DISC. In subclone TR1 pretreatment with HDACi was associated with downregulation of overexpresssed CASP10 mRNA to the levels detected in the original Jurkat cell line. Genome-wide gene-expression profiling using Illumina chips unveiled additional changes in the transcriptome associated with acquired TRAIL resistance. Across all microarrays, the most statistically significant gene expression change was upregulation of Midkine, a heparin-binding growth factor presumably involved in the protection of cancer cells against TRAIL. We showed that acquired TRAIL resistance of Jurkat T-lymphoblastic leukemia cells was associated with complex disruption of both extrinsic and intrinsic apoptotic pathways. While impaired formation of DISC appeared a major molecular mechanism underlying the death-ligand resistance of subclones TR2-3, deregulated expression of apical caspases 8 and 10 substantially contributed to resistance of subclone TR1. RNA interference experiments demonstrated downregulation of otherwise proapoptotic CASP10 functionally impaired extrinsic apoptotic pathway and results in increase apoptotic response to TRAIL. We speculate that displacement of CASP8 by overexpressed CASP10 from DISC might partially block downstream conveying of the proapoptotic signaling from aggregated death receptors. The microarray data implicated that additional molecular deregulations (e.g. overexpression of midkine) associated with acquired TRAIL resistance might contribute to the “multi-drug” resistant phenotype of TRAIL-resistant subclones. The ability of HDACi to restore sensitivity of TRAIL-resistant Jurkat subclones to TRAIL might influence design of novel experimental strategies in the treatment of cancer. Financial Support: LC 06044, MSM 0021620806, MSM 0021620808, GAUK 2009/259153/86309, GAUK 259211/110709 Disclosures: No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V114.22.3790.3790
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2009
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 6
    Online Resource
    Online Resource
    Ruptured Thoracolumbar Perimedullary Arteriovenous Fistula during Pregnancy Complicated by Cerebral Subarachnoid Hemorrhage and Brainstem Hematoma: A Case Report
    MDPI AG ; 2020
    In:  Brain Sciences Vol. 10, No. 8 ( 2020-08-15), p. 561-
    Details
    In: Brain Sciences, MDPI AG, Vol. 10, No. 8 ( 2020-08-15), p. 561-
    Abstract: Intradural spinal arteriovenous fistulas (sAVF) are spinal vascular lesions that usually manifest due to myelopathy or local symptoms caused by venous congestion and ischemia. In addition, perimedullary arteriovenous fistulas (PMAVF) in particular may rupture and cause subarachnoid or intramedullary hemorrhage along with relevant symptoms. Subarachnoid hemorrhage (SAH) can propagate into cranial space with clinically dominant symptoms and signs of typical aneurysmal intracranial SAH. The standard workup for cerebral SAH, after excluding an intracranial source of hemorrhage, is usually limited to a cervical spine MRI; therefore, thoracolumbar sources of hemorrhage can be missed, or their diagnosis may be delayed. Here we present a case of a pregnant patient who presented with cerebral SAH. The source of hemorrhage was not initially identified, leading to a presumptive diagnosis of benign pretruncal non-aneurysmal SAH. The correct diagnosis of spinal thoracolumbar PMAVF was revealed 2.5 months later due to the progression of local symptoms. While the diagnosis was being refined and endovascular treatment was being planned (but delayed due to pregnancy), there was a recurrence of intraconal hemorrhage followed by brainstem hemorrhage. This led to significant clinical deterioration. The PMAVF was then treated microsurgically and the patient experienced partial recovery.
    Type of Medium: Online Resource
    ISSN: 2076-3425
    URL: Article
    DOI: 10.3390/brainsci10080561
    Language: English
    Publisher: MDPI AG
    Publication Date: 2020
    detail.hit.zdb_id: 2651993-8
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 7
    Online Resource
    Online Resource
    CTNI-70. LONG-TERM SURVIVAL IN GLIOBLASTOMA PATIENTS AFTER TUMOR TREATING FIELDS (TTFIELDS) THERAPY
    Oxford University Press (OUP) ; 2020
    In:  Neuro-Oncology Vol. 22, No. Supplement_2 ( 2020-11-09), p. ii58-ii59
    Details
    In: Neuro-Oncology, Oxford University Press (OUP), Vol. 22, No. Supplement_2 ( 2020-11-09), p. ii58-ii59
    Abstract: Glioblastoma multiforme (GBM) is the most common and malignant primary intracranial tumor and traditionally has a median survival of only 10 to 14 months, with only 3 to 5% of patients surviving more than three years. Recurrence (RGBM) is nearly universal, and further decreases the median survival to only 5 to 7 months with optimal therapy. Thus, advances in treatment that may improve survival in these patients are highly desirable. METHODS Tumor treating fields (TTFields) therapy (Novocure Ltd., Haifa, Israel) is an approved antimitotic treatment for patients with newly diagnosed and recurrent GBM. TTFields are low-intensity (1–3 V/cm), intermediate-frequency (100–300 kHz) alternating electric fields that selectively kill or arrest the growth of rapidly dividing cells by inhibiting the proper formation of the mitotic spindle and by causing rapid membrane breakdown during cytokinesis. RESULTS Our center was the first in the world to apply TTFields treatment to histologically proven GBM in a pilot study of 20 individuals (10 GBM and 10 RGBM) in 2004 and 2005, and 4 of the original 20 patients are still alive today (2 GBM, 2 RGBM), in good health and no longer receiving any treatment roughly 15 years (range 14.2–15.9 years) after initiating TTFields therapy, with no clinical or radiological evidence of recurrence. The diagnosis of GBM was confirmed in all patients in two independent laboratories. Two of the 4 surviving patients exhibited radiological signs of tumor growth initially, before the tumor regressed in size after a median of 4 months of continuous treatment. CONCLUSIONS Our results indicate that TTFields treatment may be remarkably successful for both newly diagnosed and recurrent GBM patients. We recommend that TTFields treatment should be applied for a sufficient amount of time, and that initial radiologic progression following treatment initiation should not be considered a reason to discontinue treatment.
    Type of Medium: Online Resource
    ISSN: 1522-8517 , 1523-5866
    URL: Article
    DOI: 10.1093/neuonc/noaa215.236
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2020
    detail.hit.zdb_id: 2094060-9
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 8
    Online Resource
    Online Resource
    CTNI-73. OVERALL SURVIVAL OF NEWLY DIAGNOSED GLIOBLASTOMA PATIENTS TREATED BY STANDARD THERAPY IN COMPARISON TO STANDARD THERAPY PLUS TUMOR TREATING FIELDS
    Oxford University Press (OUP) ; 2020
    In:  Neuro-Oncology Vol. 22, No. Supplement_2 ( 2020-11-09), p. ii59-ii59
    Details
    In: Neuro-Oncology, Oxford University Press (OUP), Vol. 22, No. Supplement_2 ( 2020-11-09), p. ii59-ii59
    Abstract: Tumor treating fields (TTFields; 200 kHz) have shown significant prolonged survival in newly diagnosed (ndGBM). TTFields are anti-mitotic, low intensity, intermediate frequency alternating electric fields. The applied fields disrupt the mitotic spindle, microtubule assembly and the segregation of intracellular organelles during cell division, leading to apoptosis or mitotic arrest. We compared overall survival (OS) between patients recently treated with standard therapy and standard therapy plus TTFields at our institution. METHODS Subjects (N=25) with ndGBM treated with standard therapy plus TTFields (STDTh-TTF) at our institution were included. Standard therapy (STDTh) consisted of surgical resection, followed by combined radiotherapy and chemotherapy (Temozolomide). In 3 cases, biopsies were performed instead of resection. The date of resection or biopsy was considered the entry date and was used in calculating survival. The study took place from July 2015 to April 2019. A matching control group of 25 subjects with ndGBM were treated with STDTh alone at our institution and were assembled from our database based primarily on date of resection or biopsy, and secondarily by age (2 subjects underwent biopsy in place of resection). When assembling the control group, the investigators were blinded to survival outcome. RESULTS Significantly greater overall survival was observed for the group treated by TTFields in addition to standard therapy (p & lt; 0.001; Hazard ratio [HR] 0.21; 95% confidence interval [CI] 0.1–0.45; median survival time STDTh-TTF 31.7 months, STDTh 7.1 months). The groups were balanced with respect to sex, and no differences with respect to age (p = 0.13; STDTh-TTF mean 51.58 years, SD 8.8; STDTh mean 52.42 years, SD 8.7) or inclusion date (p = 0.22) by paired t-test were detected. CONCLUSIONS Our initial results appear promising with respect to overall survival benefit in patients undergoing TTFields treatment in addition to standard therapy.
    Type of Medium: Online Resource
    ISSN: 1522-8517 , 1523-5866
    URL: Article
    DOI: 10.1093/neuonc/noaa215.239
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2020
    detail.hit.zdb_id: 2094060-9
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 9
    Online Resource
    Online Resource
    NIMG-03. QUANTITATIVE MR MEASUREMENTS IN GLIOBLASTOMA PATIENTS: DIFFERENCE IN MEAN DIFFUSIVITY BETWEEN OPTUNE PATIENTS AND PATIENTS WITH ONLY STANDARD TREATMENT
    Oxford University Press (OUP) ; 2017
    In:  Neuro-Oncology Vol. 19, No. suppl_6 ( 2017-11-06), p. vi143-vi143
    Details
    In: Neuro-Oncology, Oxford University Press (OUP), Vol. 19, No. suppl_6 ( 2017-11-06), p. vi143-vi143
    Type of Medium: Online Resource
    ISSN: 1522-8517 , 1523-5866
    URL: Article
    DOI: 10.1093/neuonc/nox168.584
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2017
    detail.hit.zdb_id: 2094060-9
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 10
    Online Resource
    Online Resource
    Significant Brain Oedema in Unruptured Brain Arteriovenous Malformation – a Case Repor
    Care Comm ; 2017
    In:  Česká a slovenská neurologie a neurochirurgie Vol. 80/113, No. 3 ( 2017-5-31), p. 350-352
    Details
    In: Česká a slovenská neurologie a neurochirurgie, Care Comm, Vol. 80/113, No. 3 ( 2017-5-31), p. 350-352
    Type of Medium: Online Resource
    ISSN: 1210-7859 , 1802-4041
    URL: Article
    DOI: 10.14735/amcsnn2017350
    Language: Unknown
    Publisher: Care Comm
    Publication Date: 2017
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
Nothing or not found what you are looking for? Please check your search query or use the Interlibrary Loan Search.
Close ⊗
This website uses cookies and the analysis tool Matomo. Further information can be found on the KOBV privacy pages