Translation of "Zelluntergang" in English

These diseases often start with cell atrophy in the hippocampus.

The autoantibodies lead to a functional damage but not to cell destruction.

EPO ensures through this binding that cell death is limited and that cell regeneration takes place.

In a stroke, oxygen deficiency and excessive concentrations of neurotransmitters cause extensive cell death in the brain.

Although the pathogenesis of ALS is not completely elucidated, it is suggested that glutamate (the primary excitatory neurotransmitter in the central nervous system) plays a role for cell death in the disease.

It is known, that after a cardiac infarction, leucocytes migrate into the injured area and the cell destruction is accompanied by an increased releasing of the above named oxygen metabolites.

This leads into the second, decompensated shock phase, which is characterized by progressive cell death and loss of function.

In the course of wider pharmacological screening, it was additionally possible to show that the compounds of the formula I were additionally able to inhibit ischemically-related cell death in the central nervous system in a lasting manner.

It is known, that after a cardiac infarction, leucocytes migrate into the injured area and the cell destruction is accompanied by an increased releasing of the above named oxygen metabolites.

Why the mutation “only” causes cell death in the pancreas and in the brain is still unclear.

The compounds of the present invention, as a result of their NHE3-inhibitory effect, are able to preserve the cellular energy reserves which are rapidly exhausted during toxic and pathogenic events and thus lead to cell damage or cell death.

Cell destruction is traditionally evaluated in plasma (“static” tests) on the basis of the release of more or less specific hepatocellular enzymes (for example (ASAT, ALAT, GLDH, etc.).

With advancing myocardial ischemia, cell death of the cardiocytes ensues owing to “random” (necrosis) and “programmed” (apoptosis) cell death, with the necrotic swelling of the cells leading to the break-up of the cell membranes with release of the cytoplasmic constituents responsible for the inflammatory response.

During a violent, non-apoptotic cell death, phagocytes (so-called micro and macrophages) are responsible for cellular debris disposal.

Particularly in melanoma cells, betulic acid appears to specifically induce an apoptotic cell destruction in tumor cells, while melanocytes are largely resistant to this substance.

It is an activator of reactions which lead to programmed cell death (apoptosis) (Geilen, Barz and Bektas, 2001).

It does not provide any information as to whether an active substance influences the dopaminergic cell destruction at the root of the symptoms.

Therefore, there is a desire for neuroprotective substances that are able to stop or even reverse dopaminergic cell destruction (Vila et al, Nat Rev Neurosci.

Sofar, the relentless disease progression cannot be halted or stopped by any medication, however, with increasing understanding of cell death mechanisms in MSA novel strategies will become available.

The initial cell destruction, which sets in after the implantation, is limited, and, after a short time, implanted tissue can assume the intended function.

In preclinical models as well as clinical trials we explore mechanisms by which brain ischemia leads to cell death, and develop novel methods to intercept mechanisms of damage in acute brain damage, as well as to foster regeneration and repair of the lesions.

Antiphosphatidylserine antibodies (APS) have been found in pathologic pregnancies (e.g. habitual abortion) and neurologic disorders (e.g. stroke), which are associated with ischemia and apoptotic cell death as well.