Chlamydiae are gram negative, obligate intracellular bacteria, and Chlamydia trachomatis is the etiologic agent of the most commonly reported sexually transmitted disease in the United States. Chlamydiae undergo a biphasic life cycle that takes place inside a parasitophorous vacuole termed an inclusion. Chlamydial infections have been epidemiologically linked to cervical cancer in patients previously infected by human papillomavirus (HPV). The inclusion associates very closely with host cell centrosomes, and this association is dependent upon the host motor protein dynein. We have previously reported that this interaction induces supernumerary centrosomes in infected cells, leading to multipolar mitotic spindles and inhibiting accurate chromosome segregation. Our findings demonstrate that chlamydial infection causes mitotic spindle defects independently of its effect on centrosome amplification. We show that chlamydial infection increases centrosome spread and inhibits the spindle assembly checkpoint delay to disrupt centrosome clustering. These data suggest chlamydial infection exacerbates the consequences of centrosome amplification by inhibiting the cells’ ability to suppress the effects of these defects on mitotic spindle organization. We hypothesize that these combined effects on mitotic spindle architecture identifies a possible mechanism for Chlamydia as a cofactor in cervical cancer formation.

Comparisons of measurement characteristics were made for three types of electronic pain scales: (a) visual analogue scale (VAS), (b) VAS combined with an electronic number box (VAS-N; 0-100), and (c) electronic number box scale (NUM). The three scales were capable of discriminating pain sensations from very small (0.5 degrees C) temperature steps in 13 healthy males, 26 healthy females, and 16 female fibromyalgia (FM) patients. All scales provided monotonic functions when used by subjects to rate pain from 5s nociceptive temperatures (45-49 degrees C), thereby demonstrating the generality of these results across different demographic groups. As expected, FM patients rated heat pain sensations higher on all scales in comparison to healthy females, demonstrating the capacity of these scales to detect well-established group differences in pain sensitivity that exist across these two groups. However, in comparison to male subjects, healthy females gave higher NUM but not VAS or VAS-N ratings to the range of nociceptive presented temperatures. We interpret this difference as a selective scaling bias of female subjects for NUM. Finally, all three groups (total of 55 subjects) found the scales easy to use after brief instructions, though subjects strongly preferred the use of VAS-N or VAS in comparison to NUM scale.

Our data suggest that Calr specifically at HIEL may act in a non-ER dependent manner to regulate arteriolar heterocellular communication and blood pressure.