Biomedical subjects

Juergen Kempf

Publications and source records attributed to Juergen Kempf.

4 recordsLinked to original sources

PubMed2007

Detection of Delta9-tetrahydrocannabinolic acid A in human urine and blood serum by LC-MS/MS.

Delta9-tetrahydrocannabinolic acid A (Delta9-THCA-A) is the precursor of Delta9-tetrahydrocannabinol (Delta9-THC) in hemp plants. During smoking, the non-psychoactive Delta9-THCA-A is converted to Delta9-THC, the main psychoactive component of marihuana and hashish. Although the decarboxylation of Delta9-THCA-A to Delta9-THC was assumed to be complete--which means that no Delta9-THCA-A should be detectable in urine and blood serum of cannabis consumers--we found Delta9-THCA-A in the urine and blood serum samples collected from police controls of drivers suspected for driving under the influence of drugs (DUID). For LC-MS/MS analysis, urine and blood serum samples were prepared by solid-phase extraction. Analysis was performed with a phenylhexyl column using gradient elution with acetonitrile. For detection of Delta9-THCA-A, the mass spectrometer (MS) (SCIEX API 365 triple-quadrupole MS with TurboIonSpray source) was operated in the multiple reaction monitoring (MRM) mode using the following transitions: m/z357 --> 313, m/z357 --> 245 and m/z357 --> 191. Delta9-THCA-A could be detected in the urine and blood serum samples of several cannabis consumers in concentrations of up to 10.8 ng/ml in urine and 14.8 ng/ml in serum. The concentration of Delta9-THCA-A was below the Delta9-THC concentration in most serum samples, resulting in molar ratios of Delta9-THCA-A/Delta9-THC of approximately 5.0-18.6%. Only in one case, where a short elapsed time between the last intake and blood sampling is assumed, the molar ratio was 18.6% in the serum. This indicates differences in elimination kinetics, which need to be investigated in detail.

Blood Chemical Analysis↗

PubMed2005

T Cell Immunity and Aging.

The effect of age on the immune system is generally detrimental and results in "immunosenescence," a poorly-defined state inadequately reflected in clinical data and for which few reliable "biomarkers of aging" are available. The multinational consortium "T-Cell Immunity in Ageing," T-CIA, was set up to examine these issues specifically as applied to T lymphocytes. This Perspective discusses some of the outcomes of a recent conference that considered progress toward resolving these questions in humans.

Aging↗

PubMed2005

T-CIA: investigating T cells in aging.

Over the past few decades it has become clear that the immune system and especially T cells are instrumental in achieving a long and healthy life. The European Union (EU) previously supported several pan-European research projects coordinated from Tuebingen, Germany, aimed at providing a better understanding of immunosenescence. For 3 years, until the end of 2005, the EU is supporting a project called T cells in aging (T-CIA). The aim of T-CIA is to spy out and combine current efforts in immunology, molecular biology, and gerontology for a better understanding of why the elderly often have dysregulated immune responses and are more susceptible to infections and cancer.

Aging↗

PubMedDate not supplied

The heat shock proteins in cellular aging: is zinc the missing link?

T-cell functions are critical for the efficiency of the adaptive immune response. It is now clear that aging is associated with changes in the T-cell response to antigenic stimulation, one of the many changes collectively resulting in immune senescence. Several hypotheses have been proposed to explain such changes. We believe that chronic stimulation of T-cells enhances the appearance of apoptosis-resistant anergic dysfunctional cells; in humans in vivo these are predominantly specific for antigens of persistent viruses, especially CMV. Concomitantly, age-associated zinc deficiency is common and one hypothesis is that lack of zinc bioavailability contributes to impaired T-cell function. This could further compromise the integrity of T-cells under chronic antigenic stress, which can be modelled in long-term clonal cultures in vitro. Newly synthesized heat-shock proteins (HSPs) protect the cellular proteins from degradation under such conditions. In this short review we will briefly outline the role of heat-shock proteins and zinc deficiency in aging in order to finally discuss our own results in the context of a link between HSPs, aging and zinc.

Aging↗