Atomic force microscopy examination of tobacco mosaic virus and virion RNA

The majority of early-onset familial Alzheimer's disease (FAD) is associated with mutations in the presenilin-1 (PS1) gene. We describe a novel Polish PS1 mutation of Pro117Leu, associated with the earliest average age of onset and death so far reported in a PS-linked, FAD kindred. Human kidney 293 and mouse neuroblastoma N2a cells were stably transfected with wild-type and PS1 P117L. There was a significant increase in the amyloid beta42/40 ratio in the N2a P117L PS1 transfected cells compared with N2a transfected with wild-type PS1. What role PS has in the pathogenesis of AD remains to be determined, however, the severity of the clinical picture associated with this PS1 mutation stresses the importance of presenilin.     

Evaluation of the cellulolytic capacity of Ascobolus furfuraceus (Fungi, Ascomycotina)

Growth kinetic variables (dry weight, mycelial protein, extracellular protein and pH evolution) were measured in Ascobolus furfuraceus cultures either with soluble cellulose (CMC) or crystalline cellulose as only carbon sources. When growing on CMC the mycelial protein production reached a maximum at 14 days, while the extracellular protein was maximal at 17 days. On crystalline cellulose more delay was observed (4 and 14 days, respectively). Straight lineal correspondence (r = 0.9883) was observed between the extracellular protein production and enzymatic activity kinetics, showing parallel behavior of these variables. When the biomass and extracellular protein production rates were analysed, the maxima were observed at diverse growth stages. For CMC, the dry weight production rythm precedes the cellulolytic system liberation rythm (maxima at 9 and 14 days, respectively). When crystalline cellulose was the substrate, the maximal rates were inverse, 16th day for biomass production rythm and 12th day for enzyme release rythm. On the basis of such tests and analyses, a model to explain cellulose degration by A. furfuraceus, is proposed.     

Effect of clonidine on changes in plasma catecholamine concentrations and oxygen consumption caused by the cold pressor test

A range of different drugs can cause renal problems, and reactions to the radiocontrast material administered for diagnostic tests are well known. This review describes factors that put patients at risk of kidney damage from drug use and outlines how to clinically diagnose adverse reactions. The most appropriate way to deal with drug-induced renal toxicity is through prevention.     

Short duration of neutralizing antibody titers after pre-exposure rabies vaccination with suckling mouse brain vaccine

OBJECTIVE: To determine whether a Pasteurella haemolytica A1 mutant that is unable to produce membrane lipoproteins has reduced susceptibility to complement-mediated killing, and to characterize the mutant strain. SAMPLE POPULATION: 12 sera from cattle resistant to P haemolytica challenge exposure after vaccination with P haemolytica or its antigens, or after natural exposure. PROCEDURES: Complement-mediated killing assays were performed, using wild-type and mutant strains and, as antibody source, various immune sera from cattle that were resistant to P haemolytica challenge exposure. Antibody response to whole-cell antigens produced by mutant and wild-type strains, production of outer membrane proteins and iron-regulated outer membrane proteins by the 2 strains, and growth of the 2 strains in various media were analyzed. RESULTS: Compared with wild-type P haemolytica, the lipoprotein mutant strain had increased susceptibility to bovine complement-mediated killing. Aside from the lipoproteins that are not produced by the mutant, immunoblot analysis did not reveal differences between immunoreactive antigens that are produced by the 2 strains. Some iron-regulated, outer membrane proteins, which usually are only produced by P haemolytica under iron-deficient conditions, were produced constitutively by the mutant. The mutant grew to a lower final cell density and at a lower rate under conditions likely to reflect those encountered in vivo. CONCLUSIONS: Lack of 3 membrane lipoproteins resulted in enhanced susceptibility to bovine complement-mediated killing. Site-specific mutagenesis of genes encoding P haemolytica membrane lipoproteins alters production of iron-regulated outer membrane proteins by P haemolytica. Growth characteristics of the mutant suggested that it may have reduced capacity for survival in vivo.     

Effect of magnesium sulphate on adriamycin-induced clastogenic and biochemical changes in Swiss albino mice

Magnesium sulphate (magnesium), an essential anti-oxidant macromineral, was evaluated for its effects on the clastogenic and biochemical changes induced by Adriamycin (ADM) in Swiss albino mice. Male mice were treated orally with different doses (125, 250 and 500 mg/kg body weight/day) of magnesium sulphate for 7 days. Some of these mice were injected intraperitoneally with ADM (8 mg/kg body weight). Multiple sampling (12, 24 and 48 h) were carried out after the last treatment in different experiments. The animals were sacrificed under ether anaesthesia. The concentrations of magnesium were determined in plasma and liver tissue. Femoral marrow cells were collected and screened for the frequency of micronuclei and the ratio of polychromatic erythrocytes to normochromatic erythrocytes. Furthermore the proteins, nucleic acids, malondialdehyde (MDA) and non-protein sulphydryl (NPSH) levels were estimated in hepatic cells. The magnesium sulphate treatment did not affect the magnesium concentrations in plasma and liver tissue. The treatment also failed to cause any significant clastogenic, cytotoxic and biochemical changes. Pretreatment with magnesium sulphate showed no alterations in plasma and hepatic tissue levels of magnesium. Nevertheless the pretreatment was found to inhibit the ADM-induced micronuclei without any alteration in its therapeutic efficacy. The proteins, DNA, RNA and MDA levels in the hepatic cells of these animals were increased and the NPSH concentrations were reduced. The anticlastogenic nature of magnesium sulphate appears to be related to its pretreatment which might have averted the free-radical-mediated pathogenesis induced by ADM.     

The effect of long-term Enduracin monotherapy on the clinical and biochemical status of patients with ischemic heart disease

13 patients aged 39 to 60 years with coronary atherosclerosis confirmed at selective coronary angiography combined with primary hyperlipidemia (phenotypes 2a and 2b) received enduracin in a dose 1500 mg/day. As a result of the treatment total cholesterol (TC) and LDL cholesterol lowered by 10.3 and 13.1%, respectively, whereas HDL cholesterol rose by 15.2%. Half of the patients demonstrated activation of hepatic transaminases, but discontinuation of the drug was not necessary. In 3 out of 4 patients after 2 years of enduracin treatment stabilization of atherosclerosis was observed. Thus, long-term enduracin is able to inhibit progression of atherosclerosis in coronary heart disease patients.