ABSTRACT
Whipple's disease is a chronic, multisystem disease that is caused by Tropheryma whippelii infection. More information is now known about this unusual infectious process, which was once considered uniformly fatal. Immunologic, diagnostic, and therapeutic advancements are reviewed in this article. Hopefully, future advances in the basic and clinical sciences will lead to a more rapid diagnosis, more complete understanding of the effects of infection, improved therapy, and better clinical outcome.
Subject(s)
Actinomycetales Infections , Whipple Disease , Actinobacteria/isolation & purification , Actinomycetales Infections/diagnosis , Actinomycetales Infections/drug therapy , Actinomycetales Infections/history , Anti-Bacterial Agents/therapeutic use , History, 20th Century , Humans , Male , Middle Aged , Recurrence , Whipple Disease/diagnosis , Whipple Disease/drug therapy , Whipple Disease/history , Whipple Disease/microbiologyABSTRACT
The recently developed controlled cortical impact model of brain injury in rats may be an excellent tool by which to attempt to understand the neurochemical mechanisms mediating the pathophysiology of traumatic brain injury. In this study, rats were subjected to lateral controlled cortical impact brain injury of low grade severity; their brains were frozen in situ at various times after injury to measure regional levels of lactate, high energy phosphates, and norepinephrine. Tissue lactate concentration in the injury site left cortex was increased in injured animals by sixfold at 30 min and twofold at 2.5 h and 24 h after injury (p < 0.05). At all postinjury times, lactate concentration was also increased in injured animals by about twofold in the cortex and hippocampus adjacent to the injury site (p < 0.05). No significant changes occurred in the levels of ATP and phosphocreatine in most of the brain regions of injured animals. However, in the primary site of injury (left cortex), phosphocreatine concentration was decreased by 40% in injured animals at 30 min after injury (p < 0.05). The norepinephrine concentration was decreased in the injury site left cortex of injured animals by 38% at 30 min, 29% at 2.5 h, and 30% at 24 h after injury (p < 0.05). The level of norepinephrine was also reduced by approximately 20% in the cortex adjacent to the injury site in injured animals. The present results suggest that controlled cortical impact brain injury produces disorder in the neuronal oxidative and norepinephrine metabolism.
Subject(s)
Brain Injuries/metabolism , Disease Models, Animal , Lactates/metabolism , Norepinephrine/metabolism , Adenosine Triphosphate/metabolism , Animals , Cerebral Cortex/metabolism , Freezing , Hippocampus/metabolism , Lactic Acid , Male , Phosphates/metabolism , Phosphocreatine/metabolism , Rats , Rats, Inbred F344 , Tissue DistributionABSTRACT
Seed protein profiles of nine diploid species (2n = 20), ten tetraploid accessions, two synthetic amphidiploids and two autotetraploids (2n = 40) were studied using SDS-polyacrylamide gel electrophoresis. While the general profiles suggested considerable homology among these taxa in spite of speciation and ploidy differences, appreciable genetic differences were present to support the existing genomic divisions and sub-divisions in the section Arachis. A high degree of relationship was indicated between the two diploid species (A. duranensis containing the A genome and A. batizocoi (ICG 8210) containing the B genome) and tetraploids A. monticola/ A. hypogaea (2n = 40) containing AABB genome. Similar relationships were recorded between the AABB synthetic amphidiploid and the profile obtained from the mixture of protein of A. duranensis and A. batizocoi, suggesting that these two diploid species were the donors of the A and B genome, respectively, to tetraploid A. monticola/A. hypogaea.
