Inactivation of alpha-ketoglutarate dehydrogenase during oxidative decarboxylation of alpha-ketoadipic acid

alpha-Ketoglutarate dehydrogenase was inactivated irreversibly and completely during oxidation of alpha-ketoadipic acid. The inactivation was revealed both in the model system with ferricyanide and in the overall reaction catalyzed by the alpha-ketoglutarate dehydrogenase complex. Neither substrate depletion nor product accumulation induced the inactivation. The results obtained were compared with recent data on the enzyme inactivation during oxidation of alpha-ketoglutaric acid. The differences in the inactivation kinetics observed with the two substrates of the enzyme were analyzed. They seem not to reflect the different mechanisms of the inactivation, but, rather, depend on the changes in the rates of the individual stages of the process.     

The replacement of accessory T-lymphocytes by synthetic peptides during the formation of splenic hematopoietic colonies

Whether accessory T cells can be replaced by the synthetic immunomodulators thymogen (Glu-Trp) and thymohexin (Arg-Lys-Asp-Val-Tyr-Arg) was studied. The latter immunomodulator was found to show a 3-fold increase in splenic colony formation after incubation of bone marrow cells with rabbit antimouse brain serum (RAMBS). The former preparation failed to show the same action. Its effect was close to that of thymocytes. When the recipients exposed to lethal irradiation were administered the RAMBS-treated bone marrow cells and one of the peptides, it was shown that in concomitant administration, thymohexin and thymocytes lost their ability to restore colony formation by RAMBS-treated bone marrow. Thymogen did not suppress the stimulating activity of thymocytes. It is suggested that the differences observed between the tested peptides in their ability to recover colony formation were determined by their structure.     

Synthesis of inositol-containing glycophospholipids

Referring to the temporomandibular joint (TMJ) of the human mandibular locomotor system, it has been asserted that displacement of the TMJ disc and inflammation of TMJ tissues are the results of acute and indirect trauma to the TMJ; on occasion this is allegedly experienced in motor vehicle accidents and commonly known as a TMJ whiplash injury. It is postulated that the TMJ whiplash injury is released in the occupant or occupants of a target vehicle when its rear end is impacted by the front end of a bullet vehicle. On the basis of detailed analyses of TMJ trauma/pain histories and TMJ magnetic resonance images, presented as circumstantial evidence in favour of the postulated TMJ whiplash injury, and detailed analyses of the mathematical biophysics of the mandibular locomotor system as well as direct experimental evidence, it is concluded that the postulated TMJ whiplash injury does not exist as a single and independent disease entity caused by motor vehicle accidents. If TMJ disc displacement and inflammation are present, they are expressions of an insidious and progressive pre-existing (pre-accident) disease entity that is comprised of TMJ synovitis/osteoarthritis (phase of inflammation with presence of immune system cells), TMJ internal derangement (phase of disc displacement and deformation with presence of proteinases), and TMJ osteoarthrosis (phase of degeneration with absence of immune system cells). For the asserted TMJ whiplash manoeuvre and ensuing injury to occur as postulated, the laws of physics and biology would have to be suspended.