Susceptibility of human and murine Chlamydia trachomatis serovars to granulocyte- and epithelium-derived antimicrobial peptides.

Four antimicrobial peptides, protegrin-1, RTD-1, cryptdin-4, and indolicidin, were tested for their ability to inhibit the in vitro growth of Chlamydia trachomatis serovars E, L2, and mouse pneumonitis (MoPn). In general, protegrin-1 was found to have the strongest anti-chlamydial activity. Overall, of the three serovars tested, L2 was the most susceptible while MoPn was the most resistant to these peptides.     

Clinical aspects of Campylobacter jejuni infections in adults.

Campylobacter jejuni is an almost ubiquitous, microaerophilic, gram-negative rod. Outbreaks have been associated with drinking raw milk or contaminated water and eating poultry. Campylobacter jejuni accounts for 3.2% to 6.1% of cases of diarrheal illness in the general population of the United States, and infected patients frequently present with abdominal pain and fever. Less frequently, C jejuni is responsible for bacteremia, septic arthritis, septic abortion, and other extraintestinal infections. Reactive arthritis, Reiter''s syndrome, the Guillain-Barré syndrome, and pancreatitis may accompany or follow C jejuni enterocolitis. Campylobacter jejuni is an important cause of diarrheal illness and is a more commonly identified stool organism than Salmonella or Shigella species. Recurrent and chronic infection is generally reported in immunocompromised hosts.     

Eosin B

The two known isomeric dibromodinitrofiuoresceins have been prepared in a fairly pure state, and their absorption spectra determined.

Commercial samples of eosin B are not 4, 5-dibromo—2, 7-dinitrofluorescein, as stated in dye indices. They are mixtures which contain other bromonitro derivatives of fluorescein as well as di-bromodinitro derivatives.

The color acid method provides a substantially reliable means of determining actual dye content with commercial samples of the dye, but the reduction method may prove decidedly misleading.     

O-alkyl lipid synthesis: the mechanism of the acyl dihydroxyacetone phosphate fatty acid exchange reaction

We have previously provided evidence for a mechanism by which acyl DHAP is converted enzymatically to O-alkyl DHAP. This mechanism involves, in part, the formation of an endiol of acyl DHAP, loss of the fatty acid by splitting of the DHAP carbon-1 to oxygen bond and the gain of a long chain fatty alcohol. It has been shown that acyl DHAP can exchange its fatty acid for one in the medium, presumably by the mediation of O-alkyl DHAP synthase. In the present investigation we have shown that the fatty acid which is gained by acyl DHAP in the exchange process retains both carboxyl oxygens, as predicted by our postulated mechanism. This reaction is exceptional because the usual action of acyl hydrolases is to cleave at the oxygen to acyl bond.     

Class II genes of the human major histocompatibility complex. The DO beta gene is a divergent member of the class II beta gene family

A novel class II beta chain gene is described. This gene, tentatively called DO beta, displays considerably less polymorphism than beta genes of the DP, DQ, and DR loci. The nucleotide sequence of the DO beta gene is strikingly similar to that of the previously identified murine A beta 2 gene. The DO beta gene displays the same exon/intron organization as other beta genes although the fifth exon and the translated portion of the sixth exon are longer than in other genes. A striking feature of the amino acid sequence deduced from the DO beta gene sequence is the pronounced hydrophobicity of the NH2-terminal region. This feature distinguishes the putative DO beta chain from other class II beta chains and raises the possibility that DO beta chains may interact with an alpha chain that is structurally different from those of the DP, DQ, and DR loci. It further suggests that the putative DO molecule may have a function different from those of other class II antigens.     

Accelerated disulfide reduction with polyunsaturated fatty acids: a mechanism of ionic channel modulation?

Summary

Polyunsaturated fatty acids (PUFAs) have been shown to modulate the activity of ionic channels by an unknown mechanism. Some channels are activated (i.e. certain delayed-rectifier, potassium channels) and others are inhibited (i.e. certain calcium, sodium and other potassium channels). We have previously demonstrated that PUFAs can act as electron carriers. It is known that ionic channels can be redox modulated. The ability of fatty acids to serve as electron shuttling agents is proportional to their unsaturation. These PUFAs cause reduction of disulfides through a superoxide radical-independent mechanism, probably related to enhanced electron delocalization. The present study shows that there is a strong correlation between the ability of a PUFA to transfer an electron to a disulfide and its reported ability to modulate ionic channels. This suggests that electron transfer could be the mechanism of PUFAs action on particular ionic channels.