Scientific and Public-Health Aspects

Multiple Chemical Sensitivity (MCS) is a phenomenon which the ENT-doctor should be familiar with. It has its roots in the description of a syndrome in 1987. A worker spilled chemicals at his workplace and from then on he reacted highly sensitive to chemicals. Today, there are many people who explain their complaints with self-suspected MCS. Various pathopysiological models have been proposed, including toxicological, immunological or behaviorial models. But no-one could be proved so far. Since controlled provocation tests have also provided unclear results, an increasing number of doctors assumes today, that MCS reflects a psychic condition. In 1996, an expert team of the WHO has suggested the renaming of MCS to "idiopathic environmental illness" (IEI). However, other doctors still assume a chemical cause. Since there are neither straightforward diagnostic methods to proof MCS, nor reliable therapeutic concepts, treatment of MCS-patients is usually difficult. The MCS-debate (somatic vs psychic causes) seems to reflect the dilemma of the medical profession today, that somatic disorders of known origin can be well treated, whereas the increasing number of psychosomatic/ somatoform disorders is often resistant to medical help. The ENT-doctor should pay attention to changes of the nasal mucous membrane, nasal resistance and the sense of smell. Moreover he should know about the peculiarities of MCS-patients. The manuscript describes the present knowledge and state of discussion with special regard to the situation in Germany

Platelets favor the outgrowth of established metastases

Abstract Despite abundant evidence demonstrating that platelets foster metastasis, anti-platelet agents have low therapeutic potential due to the risk of hemorrhages. In addition, whether platelets can regulate metastasis at the late stages of the disease remains unknown. In this study, we subject syngeneic models of metastasis to various thrombocytopenic regimes to show that platelets provide a biphasic contribution to metastasis. While potent intravascular binding of platelets to tumor cells efficiently promotes metastasis, platelets further support the outgrowth of established metastases via immune suppression. Genetic depletion and pharmacological targeting of the glycoprotein VI (GPVI) platelet-specific receptor in humanized mouse models efficiently reduce the growth of established metastases, independently of active platelet binding to tumor cells in the bloodstream. Our study demonstrates therapeutic efficacy when targeting animals bearing growing metastases. It further identifies GPVI as a molecular target whose inhibition can impair metastasis without inducing collateral hemostatic perturbations