Cefazolin experimental epilepsy: the effects of diazepam on the interictal ECoG

Diazepam i.v. injected at the dose of 5 mg/Kg on a group of 14 Rhode-Island-Red chicks was able to antagonize and prevent the interictal EEG pattern induced by cefazolin i.v. Since cefazolin epilepsy is most probably dependent on a receptorial antagonism with GABA, these data seem to confirm the GABA-ergic nature of cefazolin epilepsy.     

Relationships Between Bactericidal Effect and Inhibition of Ribonucleic Acid Nucleotidyl-transferase by Rifampicin in Escherichia coli K-12

The mechanism of action of rifampicin, an antibiotic which inhibits in vitro the polycondensation of ribonucleotides by ribonucleic acid (RNA) nucleotidyltransferase, was studied in vivo in Escherichia coli. It is argued that the inhibition of RNA nucleotidyltransferase represents the primary lesion and is responsible for the bactericidal effect. This conclusion is based on (i) the correlation between concentrations of the antibiotic which block in vivo incorporation of labeled uracil and the bactericidal concentrations, (ii) the evidence that the loss of viability of the cells immediately follows the block of RNA synthesis, and (iii) the observation that the reversal of the inhibition of RNA synthesis goes together with a reversal of the loss of viability.     

Cholesterol glucosylation–based survival strategy in Helicobacter pylori

Helicobacter pylori is a major chronic health problem, infecting more than half of the population worldwide. H. pylori infection is linked with various clinical complications ranging from gastritis to gastric cancer. The resolution of gastritis and peptic ulcer appears to be linked with the eradication of H. pylori. However, resistance to antibiotics and eradication failure rates are reaching alarmingly high levels. This calls for urgent action in finding alternate methods for H. pylori eradication. Here, we discuss the recently identified mechanism of H. pylori known as cholesterol glucosylation, mediated by the enzyme cholesterol-α-glucosyltransferase, encoded by the gene cgt. Cholesterol glucosylation serves several functions that include promoting immune evasion, enhancing antibiotic resistance, maintaining the native helical morphology, and supporting functions of prominent virulence factors such as CagA and VacA. Consequently, strategies aiming at inhibition of the cholesterol glucosylation process have the potential to attenuate the potency of H. pylori infection and abrogate H. pylori immune evasion capabilities. Knockout of H. pylori cgt results in unsuccessful colonization and elimination by the host immune responses. Moreover, blocking cholesterol glucosylation can reverse antibiotic susceptibility in H. pylori. In this work, we review the main roles of cholesterol glucosylation in H. pylori and evaluate whether this mechanism can be targeted for the development of alternate methods for eradication of H. pylori infection.     

Regional,Layer, and Cell-Type-Specific Connectivity of the Mouse Default Mode Network

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Ultrastructural changes in human leukemic cell nuclei

The ultrastructural changes of human leukemic cell nuclei have been investigated. Particular attention is paid to the alteration of the nuclear envelope and its constituents, i.e., the pores and the Zonula Nucleum Limitans which appear constantly involved in these pathologic processes. An alteration of the relationships between the components of the nuclear envelope and the chromatin itself may be responsible for the appearance of the most nuclear changes.