Publications by authors named "Dennert G"

Sex, gender and sexual orientation are diverse, as are the ways of living associated with them. The extent to which people can live a free and self-determined life according to their own body, gender, sexuality and way of life influences their social resources, opportunities for participation and discrimination and has an influence on their life situation and health. A narrative review of lesbian, gay, bisexual, transgender and intersex (LGBTI) health was conducted including international and German reviews, meta-analyses and population-based studies.

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Background: This review is the third update of the Cochrane review "Selenium for preventing cancer". Selenium is a naturally occurring element with both nutritional and toxicological properties. Higher selenium exposure and selenium supplements have been suggested to protect against several types of cancer.

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Introduction: Complementary and alternative medicine (CAM) is often used by cancer patients, yet, communication with the oncologist is poor. The objective of our study was to gather information on patients' usage of CAM, source of information, and aims, in order to derive strategies to improve the communication between physicians and patients on this topic.

Materials And Methods: An online survey was conducted by linking a standardized questionnaire to the largest internet portal for cancer patients in Germany.

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Background: This review is an update of the first Cochrane publication on selenium for preventing cancer (Dennert 2011).Selenium is a metalloid with both nutritional and toxicological properties. Higher selenium exposure and selenium supplements have been suggested to protect against several types of cancers.

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Background: In total, 40-70% of cancer patients use complementary or alternative medicine (CAM). Many of them ask for advice from non-medical practitioners (NMPs). Our aim was to investigate the attitude of NMPs regarding their treatments for cancer patients.

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Background And Purpose: Complementary and alternative medicine (CAM) is of high relevance in oncology. Only a minority of professionals feel competent in CAM. Our aim was to provide a strategy for establishing evidence-based counseling on CAM in oncology in the German health system.

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Background: Many cancer patients use complementary and alternative medicine (CAM). Most websites offering online information on CAM are not helpful for them.

Methods: We extracted decisive elements for online information on CAM by analyzing the literature on the information needs of cancer patients and on counseling cancer patients on CAM.

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Background: No comprehensive systematic review has been published since 1998 about the frequency with which cancer patients use complementary and alternative medicine (CAM).

Methods: MEDLINE, AMED, and Embase databases were searched for surveys published until January 2009. Surveys conducted in Australia, Canada, Europe, New Zealand, and the United States with at least 100 adult cancer patients were included.

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Background: Selenium is a trace element essential to humans. Higher selenium exposure and selenium supplements have been suggested to protect against several types of cancers.

Objectives: Two research questions were addressed in this review: What is the evidence for1.

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NKT cells expressing invariant T-cell receptors are an abundant cell population in the mouse liver, and much evidence has been accumulating which shows that they play an important role in immune responses in this organ. In this review, the putative function of NKT cells in autoimmune hepatitis is discussed based on results from various mouse models. Features and functions of invariant NKT cells are summarized to set the stage to explain how these cells induce liver injury following the injection of mitogen concanavalin A or NKT-cell receptor ligand alpha-GalCer.

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Contact of T lymphocytes with nicotinamide adenine dinucleotide (NAD) or ATP causes cell death that requires expression of purinergic receptor P2X(7) (P2X(7)R). T cell subsets differ in their responses to NAD and ATP, which awaits a mechanistic explanation. Here, we show that sensitivity to ATP correlates with P2X(7)R expression levels in CD4 cells, CD8 cells and CD4(+)CD25(+) cells from both C57BL/6 and BALB/c mice.

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Hepatitis C virus (HCV) infection causes acute and chronic liver disease often leading to liver cirrhosis and hepatocellular carcinoma. Numerous studies have shown that despite induction of virus specific immunity, a curative response is often not attained; this has led to the hypothesis that HCV genes modulate immunity, thereby enabling chronic infections. This study examined the effects on immune-mediated liver injury in transgenic mice expressing core protein throughout the body and bone marrow chimeras expressing core protein in either the lymphoid compartment or liver parenchyma.

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Background: Selenium supplements are frequently used by cancer patients. Selenium is an essential trace element and is involved in antioxidant protection and redox-regulation in humans. Several adverse effects of radiotherapy and chemotherapy in cancer patients as well as cellular processes that maintain chronic lymphoedema have been linked to oxidative cell damage in the human body.

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Adenine nucleotides induce danger signals in T cells via purinergic receptors, raising the question whether they exert similar effects on innate immunity. Here we show that micromolar concentrations of nicotinamide adenine dinucleotide (NAD) induce a rapid increase of annexin V staining in NKT cells in vitro, a response that requires expression of P2X(7)Rs. Consistent with this result, treatment of mice with NAD causes a temporary decrease of NKT cells in the liver and protects from Con A- and alpha-galactosylceramide-induced hepatitis, both of which require functional NKT cells.

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Although regulatory lymphocytes play an important role in the immune system, the regulation of their functions is poorly understood and remains to be elucidated. In this study we demonstrate that micromolar concentrations of the common cell metabolite NAD induce death in murine forkhead/winged helix transcription factor gene-expressing CD4+CD25+ regulatory T cells with high efficiency and within minutes. Similar, but less dramatic, effects are demonstrable with ATP and its nonhydrolysable derivative, benzoylbenzoyl-ATP.

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Background: Injection of adenoviral constructs causes liver infection prompting immunity, which suppress viral gene expression. Innate and adaptive immunity mediate these processes raising the question which pathways are the most prominent.

Methods: Adenovirus expressing the beta-galactosidase (beta-gal) gene was injected into normal and immunodeficient mice.

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Adding NAD to murine T lymphocytes inhibits their functions and induces annexin V binding. This report shows that NAD induces cell death in a subset of T cells within seconds whereas others do not die until many hours later. Low NAD concentrations (<10 microM) suffice to trigger rapid cell death, which is associated with annexin V binding and membrane pore formation, is not blocked by the caspase inhibitor Z-VADfmk, and requires functional P2X7 receptors.

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Background & Aims: Chronic alcohol abuse induces liver injury and increases the severity of viral hepatitis, but the precise mechanisms responsible are not well understood. In particular, little is known about the role of natural killer T cells in alcohol-induced liver injury. Natural killer T cells are mediators of important regulator and effector functions making use of Fas and tumor necrosis factor (TNF)-alpha in apoptosis induction.

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Viral infection of the liver causes accumulation of T cells in the infected organ, raising the question as to the signals that mediate this response. Employing an adenovirus induced hepatitis model in mice, we show that IP-10 and Mig are essential for T cell recruitment and that induction of the two chemokines occurs concomitant to production of IFNgamma. It is shown that while IFNgamma induces IP-10 and Mig in hepatocytes, for optimal chemokine induction, a co-stimulatory signal mediated by cross-linking of Fas on hepatocytes is required.

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Immune responses in the liver have been studied for more than three decades, raising intriguing questions but providing few definitive answers. Many observations pertaining to immunity in this organ are unexpected and some of them even contradictory: parenchymal cells in the liver are readily accessible to circulating lymphocytes and may function as antigen-presenting cells (APC), yet antigens expressed in the liver often fail to induce responses and may cause systemic tolerance. There are rare lymphocyte classes in the liver, yet reasons why these cells reside in this organ and why immune responses are often poor remain to be elucidated.

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The hepatitis C virus (HCV) core protein is among the most conserved proteins in HCV and is known to induce sensitization of cytotoxic T lymphocytes (CTL). Therefore, it is a prime candidate for a component of a potential HCV vaccine. The HCV core protein has, however, been reported to exert multiple effects on cell functions, raising questions as to its suitability for this purpose.

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Incubation of mouse T cells expressing the cell surface enzyme ADP ribosyltransferase with nicotinamide adenine dinucleotide (NAD) had been reported to cause ADP ribosylation of cell surface molecules, inhibition of transmembrane signaling, and suppression of immune responses. In this study, we analyze the reasons for these effects and report that contact of T cells with NAD causes cell death. Naive T cells when incubated with NAD and adoptively transferred into semiallogeneic mice fail to cause graft-vs-host disease, and when injected into syngeneic, T cell-deficient recipients do not reconstitute these mice.

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Immunity to allogeneic MHC Ags is weak in rodent livers, raising questions as to the mechanisms that might control responses in this organ. Infection with an adenovirus vector reveals that T cell-mediated immunity to nonself-Ags in the liver is self-limiting. Virus-induced liver injury decreases and coincides with disappearance of virus-specific CTL, concomitant to an increase of apoptotic T cells early after infection.

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NK cells are a relatively rare cell population in peripheral lymphoid organs but are abundant in the liver, raising questions as to their function in immune responses to infections of this organ. To investigate this, cell-mediated immunity to viral liver infection induced by a type 5, replication-defective, adenovirus was examined. It is shown that NK cells in the absence of T cells cause hepatocyte apoptosis in virus-infected livers associated with an increase in liver enzymes in the serum.

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