In Vitro Ability of the Group B Streptococci to Inhibit Gram-Positive and Gram-Variable Constituents of the Bacterial Flora of the Female Genital Tract

Objective: The purpose of this study was to analyze the ability of septicemic and nonsepticemic isolates of group B streptococci (GBS) to inhibit in vitro the principal bacterial groups found in the normal bacterial flora of the female genital tract

Interrelationships Within the Bacterial Flora of the Female Genital Tract

Analysis of 240 consecutive vaginal swabs using the compatibility profile technique revealed that only 2 bacteria have the ability to be a sole isolate and as such a candidate to be a major aerobic regulator of the bacterial flora of the female genital tract (BFFGT). Compatibility profiles of Lactobacillus and Gardnerella vaginalis have shown that these organisms shared compatibility profiling for the majority of the normal bacterial constituents of the female genital tract. Dominance disruption appears to come from the addition of compatible co-isolates and presumed loss of numerical superiority. These phenomena appear to be the keys to reregulation of BFFGT. Lactobacillus appears to be the major regulator of both G. vaginalis and anaerobic bacteria. When additional organisms are added to the bacterial flora, they may add to or partially negate the inhibitory influence of Lactobacillus on the BFFGT. Inhibitor interrelationships appear to exist between coagulase-negative staphylococci and Staphylococcus aureus and the group B streptococci (GBS) and other beta hemolytic streptococci. Facilitating interrelationships appear to exist between S. aureus and the GBS and selected Enterobacteriaceae

Ampicillin Vs. Penicillin for In Utero Therapy

The pharmacokinetics of penicillin G and ampicillin are reviewed as they pertain to their potential use in in vitro therapy

Streptococcus pneumoniae as a Cause of Salpingitis

Background: A case of pneumococcal septicemia associated with laparoscopically documented acute salpingitis is reported

Rod and Cone Pathway Signalling Is Altered in the P2X7 Receptor Knock Out Mouse

The P2X7 receptor (P2X7-R) is expressed in the retina and brain and has been implicated in neurodegenerative diseases. However, whether it is expressed by neurons and plays a role as a neurotransmitter receptor has been the subject of controversy. In this study, we first show that the novel vesicular transporter for ATP, VNUT, is expressed in the retina, verifying the presence of the molecular machinery for ATP to act as neurotransmitter at P2X7-Rs. Secondly we show the presence of P2X7-R mRNA and protein in the retina and cortex and absence of the full length variant 1 of the receptor in the P2X7-R knock out (P2X7-KO) mouse. The role of the P2X7-R in neuronal function of the retina was assessed by comparing the electroretinogram response of P2X7-KO with WT mice. The rod photoreceptor response was found to be similar, while both rod and cone pathway post-photoreceptor responses were significantly larger in P2X7-KO mice. This suggests that activation of P2X7-Rs modulates output of second order retinal neurons. In line with this finding, P2X7-Rs were found in the outer plexiform layer and on inner retinal cell classes, including horizontal, amacrine and ganglion cells. The receptor co-localized with conventional synapses in the IPL and was expressed on amacrine cells post-synaptic to rod bipolar ribbon synapses. In view of the changes in visual function in the P2X7-KO mouse and the immunocytochemical location of the receptor in the normal retina, it is likely the P2X7-R provides excitatory input to photoreceptor terminals or to inhibitory cells that shape both the rod and cone pathway response

Anti-Prion Activity of Brilliant Blue G

BACKGROUND: Prion diseases are fatal neurodegenerative disorders with no effective therapy currently available. Accumulating evidence has implicated over-activation of P2X7 ionotropic purinergic receptor (P2X7R) in the progression of neuronal loss in several neurodegenerative diseases. This has led to the speculation that simultaneous blockade of this receptor and prion replication can be an effective therapeutic strategy for prion diseases. We have focused on Brilliant Blue G (BBG), a well-known P2X7R antagonist, possessing a chemical structure expected to confer anti-prion activity and examined its inhibitory effect on the accumulation of pathogenic isoforms of prion protein (PrPres) in a cellular and a mouse model of prion disease in order to determine its therapeutic potential. PRINCIPAL FINDINGS: BBG prevented PrPres accumulation in infected MG20 microglial and N2a neural cells at 50% inhibitory concentrations of 14.6 and 3.2 µM, respectively. Administration of BBG in vivo also reduced PrPres accumulation in the brains of mice with prion disease. However, it did not appear to alleviate the disease progression compared to the vehicle-treated controls, implying a complex role of P2X7R on the neuronal degeneration in prion diseases. SIGNIFICANCE: These results provide novel insights into the pathophysiology of prion diseases and have important implications for the treatment