The relationship between excitotoxicity and oxidative stress in the central nervous system

Excitotoxicity and oxidative stress are two phenomena that have been repeatedly described as being implicated in a wide range of disorders of the nervous system. Such disorders include several common idiopathic neurological diseases, traumatic brain injury, and the consequences of exposure to certain neurotoxic agents. While there is evidence that metabolic derangements can laed to these adverse processes, and that these processes may synergize in their damaging effects, the degree of interdependence, and the causal relation between them is not clear. The intent of this review is to delineate potential mechanisms which may unit hyperexcitation to the excessive generation of reactive oxygen species. The degree of linkage between these events appears rather strong. It is likely that excitoxicity frequency leads to a pro-oxidant condition but that high rates of generation of reactive oxygen species are not invariably accompanied by a hyperexcited neuronal state Both excitoxic and ‘oxidotoxic’ states result from the failure of normal compensatory anti excitatory and antioxidant mechanisms to maintain cellular homeostatis.     

Crystallization of the Arc repressor

Arc, a represser from Salmonella phage P22 has been crystallized from ammonium phosphate at pH 8.0. The crystals form in space group P2₁2₁2₁ with $\text{a = 90.26}\text{A}\text{?}\text{, b = 52.88}\text{A}\text{?}\text{and}\text{c = 47.58}\text{A}\text{?}$. The crystals diffract to 2.2 Å resolution.     

Histopathology of hepatic and pulmonary granulomata experimentally induced with eggs of Schistosoma mansoni

Hepatic granulomata were experimentally induced in previously unexposed white mice, albino rats and golden hamsters by injecting viable exogenous eggs of Schistosoma mansoni via the mesenterico-portal system. Histopathologic studies of livers of these animals showed that the lesions were similar to those in infections resulting form exposure to cercariae as occurs naturally in Mansonian schistosomiasis. Comparable observations made of the lungs of animals that had received egg injections via their tail veins, showed striking differences with respect to timing of the occurrence of various histopathologic stages, mean size of granulomata, cellular composition and pathologic manifestations.     

Immunotyping of freshly isolated strains of Pseudomonas aeruginosa

During 1972-1982 the bacteriological study of 1391 patients with thermal burns was carried out. As the result of clinico-bacteriological studies, the occurrence of P. aeruginosa was found to increase from 39.3% to 70.5% during this period. The immunotyping of P. aeruginosa cultures isolated in 3 burn-treatment centers showed that strains belonging to immunotypes 2, 3, 7 and 3/7 were most frequently isolated from burn wounds. These strains were found to be the cause of hospital infections in burn-treatment hospitals. In connection with the data thus obtained immunological preparations intended for the prophylaxis and treatment of P. aeruginosa infection should include P. aeruginosa strains, immunotypes 2, 3, 7 and 3/7.     

Transcriptional Profiling of Whole Blood Identifies a Unique 5-Gene Signature for Myelofibrosis and Imminent Myelofibrosis Transformation

Identifying a distinct gene signature for myelofibrosis may yield novel information of the genes, which are responsible for progression of essential thrombocythemia and polycythemia vera towards myelofibrosis. We aimed at identifying a simple gene signature – composed of a few genes - which were selectively and highly deregulated in myelofibrosis patients. Gene expression microarray studies have been performed on whole blood from 69 patients with myeloproliferative neoplasms. Amongst the top-20 of the most upregulated genes in PMF compared to controls, we identified 5 genes (DEFA4, ELA2, OLFM4, CTSG, and AZU1), which were highly significantly deregulated in PMF only. None of these genes were significantly regulated in ET and PV patients. However, hierarchical cluster analysis showed that these genes were also highly expressed in a subset of patients with ET (n = 1) and PV (n = 4) transforming towards myelofibrosis and/or being featured by an aggressive phenotype. We have identified a simple 5-gene signature, which is uniquely and highly significantly deregulated in patients in transitional stages of ET and PV towards myelofibrosis and in patients with PMF only. Some of these genes are considered to be responsible for the derangement of bone marrow stroma in myelofibrosis. Accordingly, this gene-signature may reflect key processes in the pathogenesis and pathophysiology of myelofibrosis development.