LIVIVO - Search results -

Search results

Result 1 - 10 of total 29

Search options

Article: International collaboration on alcoholic liver disease and pancreatitis: opportunities.

Purohit, Vishnudutt

Journal of gastroenterology and hepatology

2006 Volume 21 Suppl 3, Page(s) S107–8

MeSH term(s)	Humans ; International Cooperation ; Liver Diseases, Alcoholic/prevention & control ; National Institutes of Health (U.S.) ; Pancreatitis, Alcoholic/prevention & control ; Research Support as Topic ; United States
Language	English
Publishing date	2006-10
Publishing country	Australia
Document type	Journal Article
ZDB-ID	632882-9
ISSN	0815-9319
ISSN	0815-9319
DOI	10.1111/j.1440-1746.2006.04579.x
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2180: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 299: Show issues

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾

Article ; Online: Emerging trends in the abuse of designer drugs and their catastrophic health effects: update on chemistry, pharmacology, toxicology and addiction potential.

Rapaka, Rao S / Purohit, Vishnudutt / Schnur, Paul / Rutter, Joni

Life sciences

2014 Volume 97, Issue 1, Page(s) 1

MeSH term(s)	Alkaloids/adverse effects ; Alkaloids/chemistry ; Alkaloids/pharmacology ; Cannabinoids/adverse effects ; Cannabinoids/chemistry ; Cannabinoids/pharmacology ; Designer Drugs/adverse effects ; Designer Drugs/chemistry ; Designer Drugs/pharmacology ; Humans ; Substance-Related Disorders/epidemiology
Chemical Substances	Alkaloids ; Cannabinoids ; Designer Drugs ; cathinone (540EI4406J)
Language	English
Publishing date	2014-02-27
Publishing country	Netherlands
Document type	Editorial
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2014.01.074
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.368: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Cannabinoid receptor-2 and HIV-associated neurocognitive disorders.

Purohit, Vishnudutt / Rapaka, Rao S / Rutter, Joni

Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology

2014 Volume 9, Issue 4, Page(s) 447–453

Abstract: Despite the wide spread use of highly active antiretroviral therapy (HAART), mild forms of HIV-associated neuro cognitive disorders (HAND) remain commonplace. HAART treated patients now show low levels of viremia and more subtle yet biologically ... ...

Abstract	Despite the wide spread use of highly active antiretroviral therapy (HAART), mild forms of HIV-associated neuro cognitive disorders (HAND) remain commonplace. HAART treated patients now show low levels of viremia and more subtle yet biologically important signs of brain macrophage and microglial activation. Adjunctive therapeutic strategies are required to eliminate HIV-1 infection and suppress immune activation and its associated neuroinflammation. In this regard, cannabinoid receptor-2(CB2) activation is a promising means to attenuate HAND by inhibiting HIV replication, down regulating inflammation, and suppressing chemokine-like activity of viral neurotoxic proteins (for example, Tat and HIV-1gp120), and thereby prevent neuronal and synaptic loss. Inhibiting even low level HIV replication can attenuate neuronal injury by decreasing the production of neurotoxins. Down regulation of inflammation by CB2 activation is mediated through blunted activation of peri vascular macrophages and microglia; decreased production of tumor necrosis factor-α, chemokines and virotoxins. Down regulated neuroinflammation can decrease blood brain barrier permeability and leukocyte infiltration resulting in reduced neuronal injury. It is suggested that CB2 agonists may further attenuate HAND in HIVinfected patients on HAART. In addition, CB2 activation may also blunt brain injury by attenuating drug addiction.
MeSH term(s)	Animals ; Blood-Brain Barrier/metabolism ; Brain/pathology ; Brain/physiopathology ; Cannabinoids/pharmacology ; Chemokines/metabolism ; Cocaine-Related Disorders/complications ; Cocaine-Related Disorders/physiopathology ; Cognition Disorders/complications ; Cognition Disorders/pathology ; Cognition Disorders/psychology ; Cognition Disorders/virology ; Dendritic Spines/pathology ; Down-Regulation ; Gene Products, tat/metabolism ; HIV/physiology ; HIV Infections/complications ; HIV Infections/metabolism ; HIV Infections/psychology ; HIV Infections/virology ; Humans ; Inflammation/complications ; Inflammation/physiopathology ; Macrophage Activation ; Nerve Degeneration/complications ; Nerve Degeneration/pathology ; Receptor, Cannabinoid, CB2/agonists ; Receptor, Cannabinoid, CB2/physiology ; Tumor Necrosis Factor-alpha/metabolism ; Viral Proteins/antagonists & inhibitors ; Virus Replication/physiology
Chemical Substances	Cannabinoids ; Chemokines ; Gene Products, tat ; Receptor, Cannabinoid, CB2 ; Tumor Necrosis Factor-alpha ; Viral Proteins
Language	English
Publishing date	2014-07-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	2227405-4
ISSN	1557-1904 ; 1557-1890
ISSN (online)	1557-1904
ISSN	1557-1890
DOI	10.1007/s11481-014-9554-0
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Details ▾
- Full text online
- Order with fees

Book: Alcohol, tobacco, and cancer

Cho, C.-H / Purohit, Vishnudutt

2006

Author's details	editors, Chi Hin Cho, Vishnudutt Purohit
MeSH term(s)	Neoplasms/etiology ; Ethanol/adverse effects ; Tobacco/adverse effects ; Alcohol Drinking/adverse effects ; Smoking/adverse effects ; Risk Factors
Language	English
Size	viii, 312 p. :, ill.
Publisher	Karger
Publishing place	Basel ; New York
Document type	Book
ISBN	9783805581073 ; 3805581076
Database	Catalogue of the US National Library of Medicine (NLM)

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Introduction to the Symposium.

Purohit, Vishnudutt

Alcoholism, clinical and experimental research

1997 Volume 21, Issue 3, Page(s) 383–384

Abstract: In June 1995, the National Institute on Alcohol Abuse and Alcoholism sponsored a symposium on "Alcohol and Osteoporosis" at the Research Society on Alcoholism in Steamboat Springs, Colorado. The goals of the symposium were to: (a) disseminate current ... ...

Abstract	In June 1995, the National Institute on Alcohol Abuse and Alcoholism sponsored a symposium on "Alcohol and Osteoporosis" at the Research Society on Alcoholism in Steamboat Springs, Colorado. The goals of the symposium were to: (a) disseminate current information on the effects of alcohol on osteoporosis, both deleterious and beneficial; (b) discuss the mechanisms, direct and indirect, by which alcohol affects bone remodeling; and (c) encourage research in the area of alcohol and osteoporosis. This report provides an introduction to the problem, as well as to the three scientific presentations. Key Words: Alcohol, Osteoporosis, Bone.
Language	English
Publishing date	1997-05
Publishing country	England
Document type	Journal Article
ZDB-ID	428999-7
ISSN	1530-0277 ; 0145-6008
ISSN (online)	1530-0277
ISSN	0145-6008
DOI	10.1111/j.1530-0277.1997.tb03779.x
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 1375: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Drugs of abuse, dopamine, and HIV-associated neurocognitive disorders/HIV-associated dementia.

Purohit, Vishnudutt / Rapaka, Rao / Shurtleff, David

Molecular neurobiology

2011 Volume 44, Issue 1, Page(s) 102–110

Abstract: Although the incidence of HIV-associated dementia (HAD) has declined, HIV-associated neurocognitive disorders (HAND) remain a significant health problem despite use of highly active antiretroviral therapy. In addition, the incidence and/or severity of ... ...

Abstract	Although the incidence of HIV-associated dementia (HAD) has declined, HIV-associated neurocognitive disorders (HAND) remain a significant health problem despite use of highly active antiretroviral therapy. In addition, the incidence and/or severity of HAND/HAD are increased with concomitant use of drugs of abuse, such as cocaine, marijuana, and methamphetamine. Furthermore, exposure to most drugs of abuse increases brain levels of dopamine, which has been implicated in the pathogenesis of HIV. This review evaluates the potential role of dopamine in the potentiation of HAND/HAD by drugs of abuse. In the brain, multiplication of HIV in infected macrophages/microglia could result in the release of HIV proteins such as gp120 and Tat, which can bind to and impair dopamine transporter (DAT) functions, leading to elevated levels of dopamine in the dopaminergic synapses in the early asymptomatic stage of HIV infection. Exposure of HIV-infected patients to drugs of abuse, especially cocaine and methamphetamine, can further increase synaptic levels of dopamine via binding to and subsequently impairing the function of DAT. This accumulated synaptic dopamine can diffuse out and activate adjacent microglia through binding to dopamine receptors. The activation of microglia may result in increased HIV replication as well as increased production of inflammatory mediators such as tumor necrosis factor (TNF)-alpha and chemokines. Increased HIV replication can lead to increased brain viral load and increased shedding of HIV proteins, gp120 and Tat. These proteins, as well as TNF-alpha, can induce cell death of adjacent dopaminergic neurons via apoptosis. Autoxidation and metabolism of accumulated synaptic dopamine can lead to generation of reactive oxygen species (hydrogen peroxide), quinones, and semiquinones, which can also induce apoptosis of neurons. Increased cell death of dopaminergic neurons can eventually lead to dopamine deficit that may exacerbate the severity and/or accelerate the progression of HAND/HAD.
MeSH term(s)	AIDS Dementia Complex/complications ; AIDS Dementia Complex/pathology ; AIDS Dementia Complex/virology ; Acquired Immunodeficiency Syndrome/complications ; Acquired Immunodeficiency Syndrome/pathology ; Acquired Immunodeficiency Syndrome/virology ; Animals ; Brain/pathology ; Disease Models, Animal ; Dopamine/metabolism ; Humans ; Illicit Drugs/adverse effects
Chemical Substances	Illicit Drugs ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2011-07-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-011-8195-z
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2411: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article: Mechanisms of alcohol-induced hepatic fibrosis: a summary of the Ron Thurman Symposium.

Purohit, Vishnudutt / Brenner, David A

Hepatology (Baltimore, Md.)

2006 Volume 43, Issue 4, Page(s) 872–878

Abstract: This report is a summary of Ron Thurman Symposium on the Mechanisms of Alcohol-Induced Hepatic Fibrosis which was organized by The National Institutes of Health in Santa Barbara, California, June 25, 2005. The Symposium and this report highlight the ... ...

Abstract	This report is a summary of Ron Thurman Symposium on the Mechanisms of Alcohol-Induced Hepatic Fibrosis which was organized by The National Institutes of Health in Santa Barbara, California, June 25, 2005. The Symposium and this report highlight the unique aspects by which drinking alcoholic beverages may result in hepatic fibrosis. Acetaldehyde, the first metabolite of ethanol, can upregulate transcription of collagen I directly as well as indirectly by upregulating the synthesis of transforming growth factor-beta 1 (TGF-beta1). Reactive oxygen species (ROS) generated in hepatocytes by alcohol metabolism can activate collagen production in hepatic stellate cells (HSCs) in a paracrine manner. Alcohol-induced hepatocyte apoptotic bodies can be phagocytosed by HSCs and Kupffer cells and result in increased expression of TGF-beta1 and subsequent HSC activation. Kupffer cells may contribute to the activation of HSCs by releasing ROS and TGF- beta1. Innate immunity may suppress hepatic fibrosis by killing activated HSCs and blocking TGF-beta1 signaling. In patients infected with hepatitis C virus (HCV), alcohol may promote hepatic fibrosis by suppressing innate immunity. HCV core and non-structural proteins contribute to HCV-induced hepatic fibrosis. Alcohol and HCV together may promote hepatic fibrosis through increased oxidative stress and upregulation of fibrogenic cytokines. The inactive aldehyde dehydrogenase (ALDH2) and the super-active alcohol dehydrogenase (ADH2) alleles may promote hepatic fibrosis through increased accumulation of acetaldehyde in the liver. Hepatic fibrosis can be reversed by inducing selective apoptosis or necrosis of activated HSCs, or by reverse trans-differentiation of activated HSCs into the quiescent phenotype.
MeSH term(s)	Animals ; Ethanol ; Humans ; Liver Cirrhosis/chemically induced
Chemical Substances	Ethanol (3K9958V90M)
Language	English
Publishing date	2006-04
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1002/hep.21107
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 1660: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Mother-to-child transmission (MTCT) of HIV and drugs of abuse in post-highly active antiretroviral therapy (HAART) era.

Purohit, Vishnudutt / Rapaka, Rao S / Shurtleff, David

Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology

2010 Volume 5, Issue 4, Page(s) 507–515

Abstract: In the pre-highly active antiretroviral therapy (HAART) era, prenatal "vertical" mother-to-child transmission (MTCT) of HIV was about 25% and exposure of pregnant mothers to drugs of abuse (illicit drugs and tobacco smoking) was a significant ... ...

Abstract	In the pre-highly active antiretroviral therapy (HAART) era, prenatal "vertical" mother-to-child transmission (MTCT) of HIV was about 25% and exposure of pregnant mothers to drugs of abuse (illicit drugs and tobacco smoking) was a significant contributory factor of MTCT. However, with the introduction of HAART, the rate of MTCT of HIV has decreased to less that 2%. But, it is estimated that currently about 5.1% of pregnant women use illicit drugs and 16.4% smoke tobacco. The residual prevalence of MTCT is of concern and may be related to this continued prevalence of substance use among pregnant mothers. In this report, we review and present evidence that supports the hypothesis that drugs of abuse do have the potential to increase MTCT of HIV in the presence of HAART. Exposure to drugs of abuse during pregnancy may increase MTCT of HIV through a variety of mechanisms that are addressed in detail including possible damage to the placenta, induction of preterm birth, and increasing maternal plasma viral load though a variety of putative mechanisms such as: (a) promoting HIV replication in monocyte/macrophages; (b) increasing the expression of CCR5 receptors; (c) decreasing the expression of CCR5 receptor ligands; (d) increasing the expression of CXCR4 receptors; (e) increasing the expression of DC-SIGN; (f) impairing the efficacy of HAART through drug-drug interaction; and (g) promoting HIV mutation and replication through non-adherence to HAART.
MeSH term(s)	Antiretroviral Therapy, Highly Active ; Female ; HIV/drug effects ; HIV Infections/drug therapy ; HIV Infections/transmission ; Humans ; Illicit Drugs/adverse effects ; Infectious Disease Transmission, Vertical/statistics & numerical data ; Pregnancy ; Prenatal Exposure Delayed Effects ; Prevalence ; Substance-Related Disorders/complications ; Substance-Related Disorders/epidemiology
Chemical Substances	Illicit Drugs
Language	English
Publishing date	2010-09-14
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2227405-4
ISSN	1557-1904 ; 1557-1890
ISSN (online)	1557-1904
ISSN	1557-1890
DOI	10.1007/s11481-010-9242-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Details ▾
- Full text online
- Order with fees

Article ; Online: Role of cannabinoids in the development of fatty liver (steatosis).

Purohit, Vishnudutt / Rapaka, Rao / Shurtleff, David

The AAPS journal

2010 Volume 12, Issue 2, Page(s) 233–237

Abstract: Emerging evidence suggests that cannabinoids play an important role in the modulation of fatty liver, which appears to be mediated via activation of cannabinoid receptors. Steatogenic agents such as ethanol and high-fat diet can upregulate the activity ... ...

Abstract	Emerging evidence suggests that cannabinoids play an important role in the modulation of fatty liver, which appears to be mediated via activation of cannabinoid receptors. Steatogenic agents such as ethanol and high-fat diet can upregulate the activity of cannabinoid 1 (CB1) receptors via increasing synthesis of endocannabinoids, 2-arachidonoylglycerol, and anandamide. CB1 receptors can also be upregulated by obesity. CB1 receptor activation results in upregulation of lipogenic transcription factor, sterol regulatory element-binding protein 1c and its target enzymes, acetyl-CoA carboxylase-1, and fatty acid synthase and concomitantly, downregulation of carnitine palmitoyltransferase-1. This leads to increased de novo fatty acid synthesis as well as decreased fatty acid oxidation, culminating into the development of fatty liver. High-fat diet, in addition to CB1 receptor activation, appears to activate CB2 receptors that may also contribute to fatty liver. In non-alcoholic fatty liver disease, CB2 receptor activation is associated with the development of fatty liver. Cannabis smoking can increase the severity of fatty liver in hepatitis C patients although the precise mechanism is unknown. As the mechanisms involved in endocannabinoid receptor signaling are being increasingly well understood and the biosynthetic regulatory elements elucidated, these present good opportunity for the pharmaceutical scientists to design drugs to treat liver diseases, including steatosis, based on the cannabinoids, endocannabinoids, and related templates.
MeSH term(s)	Animals ; Cannabinoid Receptor Modulators/physiology ; Cannabinoids/chemistry ; Cannabinoids/pharmacology ; Fatty Liver/etiology ; Fatty Liver/pathology ; Hepatitis C/complications ; Humans ; Receptor, Cannabinoid, CB1/drug effects ; Receptor, Cannabinoid, CB1/physiology ; Receptor, Cannabinoid, CB2/drug effects ; Receptor, Cannabinoid, CB2/physiology
Chemical Substances	Cannabinoid Receptor Modulators ; Cannabinoids ; Receptor, Cannabinoid, CB1 ; Receptor, Cannabinoid, CB2
Language	English
Publishing date	2010-06
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1550-7416
ISSN (online)	1550-7416
DOI	10.1208/s12248-010-9178-0
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾
- Full text online
- Order with fees

Article ; Online: Do opioids activate latent HIV-1 by down-regulating anti-HIV microRNAs?

Purohit, Vishnudutt / Rapaka, Rao S / Rutter, Joni / Shurtleff, David

Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology

2012 Volume 7, Issue 3, Page(s) 519–523

Abstract: Researchers have recently demonstrated the presence of anti-HIV-1 microRNAs (miR-28, miR-125b, miR-150, miR-223, and miR-382) in monocytes, macrophages, and CD4+ T cells, which are the primary targets of HIV infection. These miRNAs appear to regulate the ...

Abstract	Researchers have recently demonstrated the presence of anti-HIV-1 microRNAs (miR-28, miR-125b, miR-150, miR-223, and miR-382) in monocytes, macrophages, and CD4+ T cells, which are the primary targets of HIV infection. These miRNAs appear to regulate the level of infectivity of HIV-1 in the target cells, and thus have an impact on HIV-1 latency. The levels of these miRNAs are significantly higher in resting CD4+ T cells than those in active CD4+ T cells, whereas HIV-1 infectivity is greater in active than in resting CD4+ T cells. Similarly, the levels of these miRNAs are significantly higher in monocytes than in macrophages, whereas HIV-1 infectivity is greater in macrophages than in monocytes. Down-regulation or inhibition of the activity of these miRNAs can promote replication of latent HIV-1 in resting CD4+ T cells and in monocytes. Recently, morphine was shown to down regulate the expression of anti-HIV miRNAs (miRNA-28, 125b, 150, and 382) in cultured human monocytes and this effect of morphine was mediated via activation of mu opioid receptors (MOR). In addition, levels of these anti-HIV miRNAs were significantly lower in the peripheral blood mononuclear cells (PBMCs) isolated from heroin-dependent subjects than those from control subjects. These findings raise an important question: Does morphine have potential to activate latent HIV-1 in resting CD4+ T cells and macrophages, including microglia of human subjects maintained on highly active antiretroviral therapy (HAART)? Further research is required to answer this question.
MeSH term(s)	Analgesics, Opioid/adverse effects ; Analgesics, Opioid/pharmacology ; Animals ; Antiretroviral Therapy, Highly Active/methods ; Down-Regulation/drug effects ; Down-Regulation/physiology ; HIV-1/drug effects ; HIV-1/genetics ; HIV-1/metabolism ; Humans ; Leukocytes, Mononuclear/drug effects ; Leukocytes, Mononuclear/metabolism ; Leukocytes, Mononuclear/virology ; Macrophages/drug effects ; Macrophages/metabolism ; Macrophages/virology ; MicroRNAs/antagonists & inhibitors ; MicroRNAs/physiology ; Virus Latency/drug effects ; Virus Latency/genetics
Chemical Substances	Analgesics, Opioid ; MicroRNAs
Language	English
Publishing date	2012-04-17
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2227405-4
ISSN	1557-1904 ; 1557-1890
ISSN (online)	1557-1904
ISSN	1557-1890
DOI	10.1007/s11481-012-9356-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Details ▾
- Full text online
- Order with fees

To top

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

Full text online

More links

Kategorien

Order via subito