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Bacterial vaginosis (BV) is a common condition characterised by a polymicrobial disorder, with an overgrowth of several anaerobic or facultative bacteria and with a reduction or absence of lactobacillus colonisation. The prevalence of BV ranges from 4 to 64%, depending on the racial, geographic and clinical characteristics of the study population. In asymptomatic women, the prevalence varies from 12 to 25%, and similar percentages are observed in pregnant women. Although BV is associated with several adverse outcomes, such as upper genital tract infections, pelvic inflammatory disease, endometritis, preterm birth and low birthweight, many basic questions regarding the pathogenesis of BV remain unanswered. Mucosal immune system activation may represent a critical determinant of adverse consequences associated with BV. An unequal risk for BV acquisition and\or recurrence could derive from different mucosal immune host abilities and\or capability of invading microbes to produce factors that inactivate the local immune response. BV is associated with a two-fold increased risk of preterm birth, with the greatest risk when BV is present before 16 weeks of gestation (odds ratio = 7.55). This may indicate a critical period during early gestation when BV-related organisms can gain access to the upper genital tract and set the stage for spontaneous preterm labour later in gestation. The results of treatment trials for pregnant women with BV have been heterogeneous, with anywhere from an 80% reduction to a two-fold increase in preterm birth among women who received treatment. For this reason, in current clinical practice significant controversy surrounds determining not only who and when to screen but also who and how to treat. Recent evidence shows that individual genetic backgrounds can affect chemokine production. This is an interesting area for future research and could lead to trials of treatment only for women genetically predisposed to preterm birth. [ABSTRACT FROM AUTHOR]

To evaluate the safety and efficacy era new algorithm for automatic mode switching (AMS) from DDD-DDDR to DDIR, 26 patients, 16 females and 10 males, mean age 73 ± 6 years of age, affected by sinus node disease, chronotropic incompetence, and recurrent paroxysmal atrial fibrillation (PAF) received the Medtronic There DR pacemaker. The device continuously calculates, in ms, the running average of the intrinsic atrial rate (MAR) and compares the current atrial interval (CAI) with the stored MAR. When the CAI is greater than the MAR it increases by 8 ms, and when the CAI is less than the MAR, it decreases by 23 ms. When MAR ≤ 330 ms (182 beats/min), tachycardia is detected and AMS is activated. All patients had clinical evaluation, 12-lead ECG, Holter monitoring, and exercise testing after implantation and every 3 months for I year. The results were compared with the data stored in the pacemaker memory: AMS episodes number; the histogram of the last 14 episodes; and atrial electrogram recording. Twenty-two Holter recordings in 13 patients showed PAF and in all of them AMS occurred simultaneously. AMS lasted between 10 seconds and 20 hours, and MAR ranged from 195–400 beats/min. No episode of PAF and no AMS were recorded hi 39 Holter recordings in 22 patients. Appropriate AMS was confirmed in five patients by stored atrial electrogram and in nine by 12-lead ECG and pacemaker event markers. Mean atrial sensing was 2.13 ± 1.04 mV during PAF and 3.18 ± 1.46 mV during sinus rhythm. No PAF episode and no AMS were recorded during exercise testing. In conclusion, this new algorithm was very reliable, sensitive, and specific. [ABSTRACT FROM AUTHOR]

Problem: During pregnancy, an adequate inflammatory control is essential for normal intrauterine foetus development. Vascular endothelium is known to play a critical role in regulation of inflammatory processes. We hypothesize a different ability of decidual endothelial cells (DEC) compared to endothelium from other districts to respond to inflammatory stimuli. Material and Methods: DEC were isolated and activated with inflammatory stimuli and their response in term of adhesion molecules expression, vascular leakage and cytokines production was evaluated. These data were compared to the data obtained with HUVEC and microvascular endothelial cells isolated from human skin (ADMEC) and from human endometrium (UtMEC). Results: Our observations indicate that DEC: 1. express low levels of adhesion molecules after inflammatory stimulation 2. are unable to respond to classic permeabilizing stimuli 3. present a different cytokine profile. Conclusions: Our results indicate that decidual endothelium has a different resting phenotype and shows an anti-inflammatory behavior compared to other microvascular endothelium. [ABSTRACT FROM AUTHOR]

An abstract of the article "C1q Is Involved in Human Trophoblast Invasion," by C. Agostinis, L. Rizzi, F. Bossi, A. Debeus, C. Tripodo, O. Radillo, F. De Seta, R. Bulla and F. Tedesco is presented.

Problem: We have previously found that C1q is constitutively expressed by invading trophoblast and endothelial cells of decidua and contributes to vascular and tissue remodeling. Based on these findings, we sought to determine whether there were changes in the circulating level of C1q that may be used as a diagnostic and predictive marker of preeclampsia., Method of Study: We measured the levels of C1q, C4, and complement activation products in serum or plasma of normal pregnant women and preeclamptic patients from different cohorts., Results: We observed a marked decrease in the concentration of C1q associated with a reduced level of C4 in preeclamptic patients as compared to matched healthy pregnant woman but no significant difference in the circulating level of the activating products C5a and the soluble terminal complement complex sC5b-9. Analysis of serum samples collected at early phase of pregnancy from women who later developed preeclampsia failed to show a decrease in C1q level., Conclusion: The results of the present investigation demonstrate that low levels of C1q and C4 are associated with preeclampsia but cannot be used as predictive markers., (© 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Problem: Mannose-binding lectin (MBL) is an important component of the innate immunity, present at the mucosal level in vagina: a common pathogen's entry point., Method of Study: We used a rapid genotyping method based on melting temperature assay to search for three single nucleotide polymorphisms (SNPs) located in the first exon of the MBL2 gene and we also measured MBL serum levels in patients with recurrent bacterial vaginosis (rBV) and recurrent vulvovaginal candidiasis (rVVC)., Results: Detected frequencies of MBL2 SNPs were comparable to the ones already reported for the Italian population and no significant differences were found between rVVC, rBV and controls. MBL serum levels did not show significant differences between the studied groups., Conclusion: No correlation for the screened mutations has been found neither in protecting nor in favoring the infection in rVVC and rBV patients. Our data demonstrate a lack of association between functional polymorphisms in the first exon of MBL2 gene, MBL deficiency, VVC and rBV.

Problem: May anti-phospholipid or other autoantibodies interfere with trophoblast-endothelial cells interaction in women with unexplained pregnancy losses?, Methods of Study: The sera of 72 women with recurrent spontaneous abortions (RSA) containing antibodies to endothelial cells (28), trophoblast (14), and cardiolipin (10) or lacking antibodies (25), and 26 controls were examined in an inhibition assay of trophoblast adhesion to endothelial cells using an ELISA based on the recognition of trophoblast by antibodies to cytokeratin., Results: Adhesion of trophoblast to endothelial cells was time- and dose-dependent. Patients and control sera inhibited trophoblast adhesion with mean values of 37% and 7%, respectively. Inhibition above 2SD of the mean control value was still observed in 58% of the patients sera and 8% of the control sera. Sera containing antibodies to endothelial cells had higher inhibitory effect (38%) than those with antibodies to trophoblast (23%) and cardiolipin (28%) or lacking antibodies (26%)., Conclusions: Antibodies and other undefined factors in the sera of women with RSA inhibit adhesion of trophoblast to endothelial cells.