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Article ; Online: Bcl-2:Beclin 1 complex: multiple, mechanisms regulating autophagy/apoptosis toggle switch.

Marquez, Rebecca T / Xu, Liang

2012 Volume 2, Issue 2, Page(s) 214–221

Abstract: Cancer cells have developed novel mechanisms for evading chemotherapy-induced apoptosis and autophagy-associated cell death pathways. Upon the discovery that chemotherapeutics could target these cell death pathways in a manner that was not mutually ... ...

Abstract	Cancer cells have developed novel mechanisms for evading chemotherapy-induced apoptosis and autophagy-associated cell death pathways. Upon the discovery that chemotherapeutics could target these cell death pathways in a manner that was not mutually exclusive, new discoveries about the interrelationship between these two pathways are emerging. Key proteins originally thought to be "autophagy-related proteins" are now found to be involved in either inducing or inhibiting apoptosis. Similarly, apoptosis inhibiting proteins can also block autophagy-associated cell death. One example is the complex formed by the autophagy protein, Beclin 1, and anti-apoptotic protein Bcl-2, which leads to inhibition of autophagy-associated cell death. Researchers have been investigating additional mechanisms that form/disrupt this complex in order to better design chemotherapeutics. This review will highlight the role Bcl-2 and Beclin 1 play in cancer development and drug resistance, as well as the role the Bcl-2:Beclin 1 complex in the switch between autophagy and apoptosis.
Language	English
Publishing date	2012-02-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2589522-9
ISSN	2156-6976 ; 2156-6976
ISSN (online)	2156-6976
ISSN	2156-6976
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Female Genital Fibroblasts Diminish the In Vitro Efficacy of PrEP against HIV.

George, Ashley F / McGregor, Matthew / Gingrich, David / Neidleman, Jason / Marquez, Rebecca S / Young, Kyrlia C / Thanigaivelan, Kaavya L / Greene, Warner C / Tien, Phyllis C / Deitchman, Amelia N / Spitzer, Trimble L / Roan, Nadia R

Viruses

2022 Volume 14, Issue 8

Abstract: The efficacy of HIV pre-exposure prophylaxis (PrEP) is high in men who have sex with men, but much more variable in women, in a manner largely attributed to low adherence. This reduced efficacy, however, could also reflect biological factors. ... ...

Abstract	The efficacy of HIV pre-exposure prophylaxis (PrEP) is high in men who have sex with men, but much more variable in women, in a manner largely attributed to low adherence. This reduced efficacy, however, could also reflect biological factors. Transmission to women is typically via the female reproductive tract (FRT), and vaginal dysbiosis, genital inflammation, and other factors specific to the FRT mucosa can all increase transmission risk. We have demonstrated that mucosal fibroblasts from the lower and upper FRT can markedly enhance HIV infection of CD4+ T cells. Given the current testing of tenofovir disoproxil fumarate, cabotegravir, and dapivirine regimens as candidate PrEP agents for women, we set out to determine using in vitro assays whether endometrial stromal fibroblasts (eSF) isolated from the FRT can affect the anti-HIV activity of these PrEP drugs. We found that PrEP drugs exhibit significantly reduced antiviral efficacy in the presence of eSFs, not because of decreased PrEP drug availability, but rather of eSF-mediated enhancement of HIV infection. These findings suggest that drug combinations that target both the virus and infection-promoting factors in the FRT-such as mucosal fibroblasts-may be more effective than PrEP alone at preventing sexual transmission of HIV to women.
MeSH term(s)	Anti-HIV Agents/pharmacology ; Anti-HIV Agents/therapeutic use ; Female ; Fibroblasts ; HIV Infections/drug therapy ; HIV Infections/prevention & control ; Homosexuality, Male ; Humans ; Male ; Sexual and Gender Minorities ; Vagina
Chemical Substances	Anti-HIV Agents
Language	English
Publishing date	2022-08-04
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v14081723
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Female Genital Fibroblasts Diminish the In Vitro Efficacy of PrEP against HIV

George, Ashley F. / McGregor, Matthew / Gingrich, David / Neidleman, Jason / Marquez, Rebecca S. / Young, Kyrlia C. / Thanigaivelan, Kaavya L. / Greene, Warner C. / Tien, Phyllis C. / Deitchman, Amelia N. / Spitzer, Trimble L. / Roan, Nadia R.

Viruses. 2022 Aug. 04, v. 14, no. 8

2022

Abstract	The efficacy of HIV pre-exposure prophylaxis (PrEP) is high in men who have sex with men, but much more variable in women, in a manner largely attributed to low adherence. This reduced efficacy, however, could also reflect biological factors. Transmission to women is typically via the female reproductive tract (FRT), and vaginal dysbiosis, genital inflammation, and other factors specific to the FRT mucosa can all increase transmission risk. We have demonstrated that mucosal fibroblasts from the lower and upper FRT can markedly enhance HIV infection of CD4+ T cells. Given the current testing of tenofovir disoproxil fumarate, cabotegravir, and dapivirine regimens as candidate PrEP agents for women, we set out to determine using in vitro assays whether endometrial stromal fibroblasts (eSF) isolated from the FRT can affect the anti-HIV activity of these PrEP drugs. We found that PrEP drugs exhibit significantly reduced antiviral efficacy in the presence of eSFs, not because of decreased PrEP drug availability, but rather of eSF-mediated enhancement of HIV infection. These findings suggest that drug combinations that target both the virus and infection-promoting factors in the FRT—such as mucosal fibroblasts—may be more effective than PrEP alone at preventing sexual transmission of HIV to women.
Keywords	HIV infections ; antiretroviral properties ; disease prevention ; drugs ; dysbiosis ; endometrium ; female genitalia ; fibroblasts ; fumarates ; inflammation ; mucosa ; risk ; viruses
Language	English
Dates of publication	2022-0804
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2516098-9
ISSN	1999-4915
ISSN	1999-4915
DOI	10.3390/v14081723
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: A non-intrusive evaluation method for tumor-targeting characteristics of nanomedicines based on in vivo near-infrared fluorescence imaging.

Liu, Hao / Marquez, Rebecca T / Wu, Xiaoqing / Li, Ke / Vadlamani, Shweta / Li, Song / Wang, Ya / Xu, Liang / Wu, Daocheng

Journal of materials chemistry. B

2019 Volume 7, Issue 31, Page(s) 4751–4757

Abstract: We developed a novel evaluation method for tumor-targeting characteristics of nanomedicines, average tumor-targeting index (average TTI) and "area under the tumor-targeting index-time curve" (AUTC) were established as the indicators for tumor targeting ... ...

Abstract	We developed a novel evaluation method for tumor-targeting characteristics of nanomedicines, average tumor-targeting index (average TTI) and "area under the tumor-targeting index-time curve" (AUTC) were established as the indicators for tumor targeting of nanomedicines based on NIR fluorescence imaging, which helps real-time monitoring of targeting ability and tumor changes in vivo without culling animals.
MeSH term(s)	Animals ; Antineoplastic Agents/therapeutic use ; Carbocyanines/chemistry ; Cell Line, Tumor ; Drug Carriers/chemistry ; Female ; Fluorescent Dyes/chemistry ; Gossypol/therapeutic use ; Humans ; Hyaluronic Acid/chemistry ; Mice, SCID ; Micelles ; Nanoparticles/chemistry ; Neoplasms/diagnostic imaging ; Optical Imaging/methods ; Polyethyleneimine/chemistry
Chemical Substances	1,1'-dioctadecyl-3,3,3',3'-tetramethylindotricarbocyanine ; Antineoplastic Agents ; Carbocyanines ; Drug Carriers ; Fluorescent Dyes ; Micelles ; Polyethyleneimine (9002-98-6) ; Hyaluronic Acid (9004-61-9) ; Gossypol (KAV15B369O)
Language	English
Publishing date	2019-08-05
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2702241-9
ISSN	2050-7518 ; 2050-750X
ISSN (online)	2050-7518
ISSN	2050-750X
DOI	10.1039/c9tb00882a
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: A non-intrusive evaluation method for tumor-targeting characteristics of nanomedicines based on in vivo near-infrared fluorescence imaging

Liu, Hao / Marquez, Rebecca T / Wu, Xiaoqing / Li, Ke / Vadlamani, Shweta / Li, Song / Wang, Ya / Xu, Liang / Wu, Daocheng

Journal of materials chemistry B. 2019 Aug. 7, v. 7, no. 31

2019

Abstract: We developed a novel evaluation method for tumor-targeting characteristics of nanomedicines, average tumor-targeting index (average TTI) and “area under the tumor-targeting index-time curve” (AUTC) were established as the indicators for tumor targeting ... ...

Abstract	We developed a novel evaluation method for tumor-targeting characteristics of nanomedicines, average tumor-targeting index (average TTI) and “area under the tumor-targeting index-time curve” (AUTC) were established as the indicators for tumor targeting of nanomedicines based on NIR fluorescence imaging, which helps real-time monitoring of targeting ability and tumor changes in vivo without culling animals.
Keywords	animals ; chemistry ; fluorescence ; image analysis ; monitoring ; nanomedicine ; neoplasms
Language	English
Dates of publication	2019-0807
Size	p. 4751-4757.
Publishing place	The Royal Society of Chemistry
Document type	Article
ZDB-ID	2702241-9
ISSN	2050-7518 ; 2050-750X
ISSN (online)	2050-7518
ISSN	2050-750X
DOI	10.1039/c9tb00882a
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Overexpression of 17β-hydroxysteroid dehydrogenase type 10 increases pheochromocytoma cell growth and resistance to cell death.

Carlson, Emily A / Marquez, Rebecca T / Du, Fang / Wang, Yongfu / Xu, Liang / Yan, Shirley ShiDu

BMC cancer

2015 Volume 15, Page(s) 166

Abstract: Background: 17β-hydroxysteroid dehydrogenase type 10 (HSD10) has been shown to play a protective role in cells undergoing stress. Upregulation of HSD10 under nutrient-limiting conditions leads to recovery of a homeostatic state. Across disease states, ... ...

Abstract	Background: 17β-hydroxysteroid dehydrogenase type 10 (HSD10) has been shown to play a protective role in cells undergoing stress. Upregulation of HSD10 under nutrient-limiting conditions leads to recovery of a homeostatic state. Across disease states, increased HSD10 levels can have a profound and varied impact, such as beneficial in Parkinson's disease and harmful in Alzheimer's disease. Recently, HSD10 overexpression has been observed in some prostate and bone cancers, consistently correlating with poor patient prognosis. As the role of HSD10 in cancer remains underexplored, we propose that cancer cells utilize this enzyme to promote cancer cell survival under cell death conditions. Methods: The proliferative effect of HSD10 was examined in transfected pheochromocytoma cells by growth curve analysis and a xenograft model. Fluctuations in mitochondrial bioenergetics were evaluated by electron transport chain complex enzyme activity assays and energy production. Additionally, the effect of HSD10 on pheochromocytoma resistance to cell death was investigated using TUNEL staining, MTT, and complex IV enzyme activity assays. Results: In this study, we examined the tumor-promoting effect of HSD10 in pheochromocytoma cells. Overexpression of HSD10 increased pheochromocytoma cell growth in both in vitro cell culture and an in vivo xenograft mouse model. The increases in respiratory enzymes and energy generation observed in HSD10-overexpressing cells likely supported the accelerated growth rate observed. Furthermore, cells overexpressing HSD10 were more resistant to oxidative stress-induced perturbation. Conclusions: Our findings demonstrate that overexpression of HSD10 accelerates pheochromocytoma cell growth, enhances cell respiration, and increases cellular resistance to cell death induction. This suggests that blockade of HSD10 may halt and/or prevent cancer growth, thus providing a promising novel target for cancer patients as a screening or therapeutic option.
MeSH term(s)	3-Hydroxyacyl CoA Dehydrogenases/genetics ; 3-Hydroxyacyl CoA Dehydrogenases/metabolism ; Animals ; Cell Death/genetics ; Cell Line, Tumor ; Cell Proliferation ; Cyclophilins/metabolism ; Disease Models, Animal ; Gene Expression ; Heterografts ; Humans ; Membrane Potential, Mitochondrial/genetics ; Mice ; Mitochondria/metabolism ; Organelle Biogenesis ; Oxidative Stress/genetics ; Pheochromocytoma/genetics ; Pheochromocytoma/metabolism ; Pheochromocytoma/pathology ; Protein Binding ; Rats ; Transfection
Chemical Substances	3-Hydroxyacyl CoA Dehydrogenases (EC 1.1.1.-) ; HSD17B10 protein, human (EC 1.1.1.35) ; Cyclophilins (EC 5.2.1.-)
Language	English
Publishing date	2015-03-22
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1471-2407
ISSN (online)	1471-2407
DOI	10.1186/s12885-015-1173-5
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Correction to "Targeted Delivery of Doxorubicin by Folic Acid-Decorated Dual Functional Nanocarrier".

Lu, Jianqin / Zhao, Wenchen / Huang, Yixian / Liu, Hao / Marquez, Rebecca / Gibbs, Robert B / Li, Jiang / Venkataramanan, Raman / Xu, Liang / Li, Shulin / Li, Song

Molecular pharmaceutics

2019 Volume 16, Issue 9, Page(s) 4087

Language	English
Publishing date	2019-08-09
Publishing country	United States
Document type	Journal Article ; Published Erratum
ZDB-ID	2138405-8
ISSN	1543-8392 ; 1543-8384
ISSN (online)	1543-8392
ISSN	1543-8384
DOI	10.1021/acs.molpharmaceut.9b00818
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Article ; Online: Targeting the interaction between RNA-binding protein HuR and FOXQ1 suppresses breast cancer invasion and metastasis.

Wu, Xiaoqing / Gardashova, Gulhumay / Lan, Lan / Han, Shuang / Zhong, Cuncong / Marquez, Rebecca T / Wei, Lanjing / Wood, Spencer / Roy, Sudeshna / Gowthaman, Ragul / Karanicolas, John / Gao, Fei P / Dixon, Dan A / Welch, Danny R / Li, Ling / Ji, Min / Aubé, Jeffrey / Xu, Liang

Communications biology

2020 Volume 3, Issue 1, Page(s) 193

Abstract: Patients diagnosed with metastatic breast cancer have a dismal 5-year survival rate of only 24%. The RNA-binding protein Hu antigen R (HuR) is upregulated in breast cancer, and elevated cytoplasmic HuR correlates with high-grade tumors and poor clinical ... ...

Abstract	Patients diagnosed with metastatic breast cancer have a dismal 5-year survival rate of only 24%. The RNA-binding protein Hu antigen R (HuR) is upregulated in breast cancer, and elevated cytoplasmic HuR correlates with high-grade tumors and poor clinical outcome of breast cancer. HuR promotes tumorigenesis by regulating numerous proto-oncogenes, growth factors, and cytokines that support major tumor hallmarks including invasion and metastasis. Here, we report a HuR inhibitor KH-3, which potently suppresses breast cancer cell growth and invasion. Furthermore, KH-3 inhibits breast cancer experimental lung metastasis, improves mouse survival, and reduces orthotopic tumor growth. Mechanistically, we identify FOXQ1 as a direct target of HuR. KH-3 disrupts HuR-FOXQ1 mRNA interaction, leading to inhibition of breast cancer invasion. Our study suggests that inhibiting HuR is a promising therapeutic strategy for lethal metastatic breast cancer.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; ELAV-Like Protein 1/antagonists & inhibitors ; ELAV-Like Protein 1/genetics ; ELAV-Like Protein 1/metabolism ; Female ; Forkhead Transcription Factors/genetics ; Forkhead Transcription Factors/metabolism ; Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Lung Neoplasms/prevention & control ; Lung Neoplasms/secondary ; Mice, Inbred BALB C ; Mice, Nude ; Middle Aged ; Neoplasm Invasiveness ; Signal Transduction ; Tumor Burden/drug effects ; Xenograft Model Antitumor Assays
Chemical Substances	Antineoplastic Agents ; ELAV-Like Protein 1 ; ELAVL1 protein, human ; FOXQ1 protein, human ; Forkhead Transcription Factors
Language	English
Publishing date	2020-04-24
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-020-0933-1
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Article: Advances in microRNAs: implications for gene therapists.

Marquez, Rebecca T / McCaffrey, Anton P

Human gene therapy

2007 Volume 19, Issue 1, Page(s) 27–38

Abstract: MicroRNAs (miRNAs) are a class of small regulatory RNAs that are thought to regulate the expression of as many as one-third of all human messenger RNAs (mRNAs). miRNAs are thought to be involved in diverse biological processes, including tumorigenesis. ... ...

Abstract	MicroRNAs (miRNAs) are a class of small regulatory RNAs that are thought to regulate the expression of as many as one-third of all human messenger RNAs (mRNAs). miRNAs are thought to be involved in diverse biological processes, including tumorigenesis. Analysis of miRNA levels may have diagnostic implications. Evidence shows that numerous viruses interact with the miRNA machinery, and that a number of viruses encode their own miRNAs. It seems likely that miRNAs will be implicated in many human diseases. Manipulation of miRNA levels by gene therapy provides an attractive new approach for therapeutic development. This review focuses on approaches to manipulate miRNA levels in cells and in vivo, and the implications for gene therapy. Furthermore, we discuss the use of endogenous miRNAs as scaffolds for the expression of RNA interference (RNAi) as well as competition between exogenous RNAi triggers and endogenous miRNAs. Because short interfering RNAs can also act as miRNAs, seed matches with the 3' untranslated regions of genes should be avoided to prevent off-target effects. Last, we discuss the use of miRNAs to avoid immune responses to viral vectors.
MeSH term(s)	Genetic Therapy ; Genetic Vectors ; Humans ; MicroRNAs/metabolism ; Models, Biological ; Models, Genetic ; RNA Interference
Chemical Substances	MicroRNAs
Language	English
Publishing date	2007-12-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1028152-6
ISSN	1557-7422 ; 1043-0342
ISSN (online)	1557-7422
ISSN	1043-0342
DOI	10.1089/hum.2007.147
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Article ; Online: MicroRNA-383 acts as a tumor suppressor in colorectal cancer by modulating CREPT/RPRD1B expression.

Li, Jian / Smith, Amber R / Marquez, Rebecca T / Li, Jun / Li, Kun / Lan, Lan / Wu, Xiaoqing / Zhao, Linxi / Ren, Fangli / Wang, Yi / Wang, Yinyin / Jia, Baoqing / Xu, Liang / Chang, Zhijie

Molecular carcinogenesis

2018 Volume 57, Issue 10, Page(s) 1408–1420

Abstract: CREPT (Cell-cycle-related and expression-elevated protein in tumor)/RPRD1B, a novel protein that enhances the transcription of Cyclin D1 to promote cell proliferation during tumorigenesis, was demonstrated highly expressed in most of tumors. However, it ... ...

Abstract	CREPT (Cell-cycle-related and expression-elevated protein in tumor)/RPRD1B, a novel protein that enhances the transcription of Cyclin D1 to promote cell proliferation during tumorigenesis, was demonstrated highly expressed in most of tumors. However, it remains unclear how CREPT is regulated in colorectal cancers. In this study, we report that miR-383 negatively regulates CREPT expression. We observed that CREPT was up-regulated but the expression of miR-383 was down regulated in both colon cancer cell lines and colon tumor tissues. Intriguingly, we found that enforced expression of miR-383 inhibited the expression of CREPT at both the mRNA and protein level. Using a luciferase reporter, we showed that miR-383 targeted the 3'-UTR of CREPT mRNA directly. Consistently we observed that over expression of miR-383 shortened the half-life of CREPT mRNA in varieties of colorectal cancer cells. Furthermore, restoration of miR-383 inhibited cell growth and colony formation of colon cancer cells accompanied by inhibition of expression of CREPT and related downstream genes. Finally, we demonstrated that stable over expression of miR-383 in colon cancer cells decreased the growth of the tumors. Our results revealed that the abundant expression of CREPT in colorectal cancers is attributed to the decreased level of miR-383. This study shed a new light on the potential therapeutic therapy strategy for colorectal cancers using introduced miRNA.
MeSH term(s)	3' Untranslated Regions/genetics ; Aged ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cell Line ; Cell Line, Tumor ; Cell Proliferation/genetics ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; HCT116 Cells ; HEK293 Cells ; HT29 Cells ; Humans ; Male ; MicroRNAs/genetics ; Middle Aged ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; RNA Stability/genetics
Chemical Substances	3' Untranslated Regions ; Cell Cycle Proteins ; MIRN383 microRNA, human ; MicroRNAs ; Neoplasm Proteins ; RPRD1B protein, human
Language	English
Publishing date	2018-07-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1004029-8
ISSN	1098-2744 ; 0899-1987
ISSN (online)	1098-2744
ISSN	0899-1987
DOI	10.1002/mc.22866
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