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Preterm delivery complicates 5–12% of pregnancies and is the primary cause of neonatal morbidity and mortality. The pathophysiology of preterm labor and parturition is not fully known, although it is probably related to inflammation and placental senescence. Telomere shortening is related to senescence and galectin-3 (Gal-3) protein is involved in cell growth, differentiation, inflammation, and fibrosis. This study examined changes in Gal-3 expression and telomere homeostasis (which represent inflammatory and stress markers) in maternal blood and placental tissue of spontaneous preterm births (SPTB) and uncomplicated, spontaneous term pregnancies (NTP) during labor. Participants included 19 women with NTP and 11 with SPTB who were enrolled during admission for delivery. Maternal blood samples were obtained along with placental tissue for Gal-3 analysis and telomere length evaluation. Gal-3 protein expression in placental tissue was increased in SPTB compared to NTP (fold change: 1.89 ± 0.36, P < 0.05). Gal-3 immunohistochemistry demonstrated strong staining in placental extravillous trophoblast tissue from SPTB. Maternal blood levels of Gal-3 protein were elevated in SPTB compared to NTP (19.3 ± 1.3 ng/ml vs. 13.6 ± 1.07 ng/ml, P = 0.001). Placental samples from SPTB had a higher percentage of trophoblasts with short telomeres (47.6%) compared to NTP (15.6%, P < 0.0001). Aggregate formation was enhanced in SPTB (7.8%) compared to NTP (1.98%, P < 0.0001). Maternal blood and placental samples from SPTB had shorter telomeres and increased Gal-3 expression compared to NTP. These findings suggest that increased senescence and inflammation might be factors in the abnormal physiology of spontaneous preterm labor. [ABSTRACT FROM AUTHOR]

To evaluate changes in the inflammatory response of thioredoxin (TXN), thioredoxin interacting protein (TXNIP), transducer and activator of transcription 3, NFƙB-p50 and STAT3 at the level of maternal serum, placenta, and umbilical cord blood of women with gestational diabetes mellitus type 2 (GDMA2) compared to normal pregnancies (NP). Thirty pregnant women (20 with GDMA2 and 10 NP) were recruited during admission for delivery. Blood samples were obtained from the parturients and umbilical cords, as well as placental tissue for mRNA and protein extraction. TXNIP mRNA expression was significantly increased in maternal serum of women with GDMA2 compared to NP women. TXNIP mRNA was significantly decreased in GDMA2 placentas and cord blood compared to NP. TXN/TXNIP mRNA ratio showed significantly high absolute values in placental and cord blood (2.39 and 1.66) respectively, compared to maternal ratio (1.084) (P < 0.001). TXN/TXNIP placenta protein ratio showed similar values between GDMA2 and NP (0.98 and 0.86; P = 0.7). STAT3 and its target protein SOCS3, as well as NFƙB-p50 mRNA expression were significantly increased in placentas of GDMA2. NFƙB-p50 mRNA expression was significantly decreased in cord blood compared to both maternal and placental mRNA expression. Pro-inflammatory changes are expressed by low mRNA TXN/TXNIP ratio in maternal blood of GDMA2 patients, but not in placental and umbilical cord blood samples. This, as well as the feedback role of SOCS3 in STAT3 pathway and NFƙB-p50 expression, may indicate that the placenta has a role in protecting the fetus from damage due to inflammatory response, which is common in diabetes. [ABSTRACT FROM AUTHOR]

Purpose: The incidence of stroke in patients undergoing hemodialysis (HD) is eight-to-ten times greater than that of the general population. However, data on the outcome of stroke in these patients are limited. Methods: In this retrospective observational cohort study, electronic medical records of all patients undergoing HD from 1.1.2014 to 31.12.2017 at Meir Medical Center, Israel, were reviewed. Stroke was defined as a focal neurological deficit of cerebrovascular origin, and confirmed as ischemic or hemorrhagic by computed tomography. Age- and sex-matched HD patients who did not experience a stroke (HD-NS) and hospitalized stroke patients with normal kidney function (NRF-S) served as the two control groups. Baseline demographic, clinical, and laboratory data were collected. Thrombolytic therapy, duration of hospital stay, and mortality were recorded. Functional status at discharge was assessed by the Modified Rankin Scale. Results: In the cohort study group (HD-S), 52 strokes occurred during 248.3 patient years, an incidence rate of 8.13%, and a stroke rate of 0.19% patients/month. Most strokes in HD patients were ischemic, and only four patients were administered tissue plasminogen activator. HD-S had longer hospitalization than did NRF-S (10.6 ± 9.9 vs. 5.96 ± 5.3 days, p = 0.004) and lower functional status at discharge (Rankin score 3.75 ± 1.57 vs. 2.29 ± 1.89, p < 0.001). HD-S patients had a higher mortality than both HD-NS and NRF-S patients. Conclusions: Stroke outcome in these patients is dismal with prolonged hospital stay, poor functional status at discharge, very limited response to rehabilitation, and increased mortality. [ABSTRACT FROM AUTHOR]

Purpose: Evaluate the efficacy of retraining and catheter exit site care in reducing peritonitis rates. Methods: This interventional study included all prevalent PD patients from 1/2009 to 12/2017 from a single center. Peritonitis rates and causative organisms were assessed and compared in three periods: (1) Before intervention (01/2009–12/2014), (2) after educational intervention: assessment of training process by infection control nurse and repeat training every 3 months, after each peritonitis episode and after hospitalizations > 2 weeks (01/2015–02/2016), and (3) in addition to the measures in period 2, an exit site care protocol including postoperative care, topical antibacterial therapy and nasal Staph aureus screening and eradication was implemented (03/2016–12/2017). Results: The study included 201 patients (149 men, 52 women), mean age was 65.1 ± 12.6 years. After both interventions, including educational and exit site care strategies, peritonitis decreased significantly from 1.05 episodes per patient-year (n = 113) to 0.67 (n = 54); P = 0.017 between periods 1 and 3. The percentage of peritonitis-free patients increased from 27.4 to 52.4 and 55.6%, respectively (P = 0.001 between period 1 vs. 2 and period 1 vs. 3.). Coagulase-negative staph was the most common pathogen, causing 7.56 peritonitis episodes per year, followed by pseudomonas at 4.33 episodes annually and staph aureus at 3.44 episodes per year. Conclusions: Enforcement of an educational program and strict adherence to an exit site care protocol was associated with a significant decrease in peritonitis rates. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate (a) the properties of high-density lipoproteins (HDL)/cholesterol, which include apolipoprotein A-1 (ApoA1) and paraoxonase1 (PON1), both are negative predictors of cardiovascular risk and (b) HDL function, among women with preeclampsia (PE). PE is a multi-system disorder, characterized by onset of hypertension and proteinuria or other end-organ dysfunction in the second half of pregnancy. Preeclampsia is associated with increased risk for later cardiovascular disease. The inverse association between HDL, cholesterol levels and the risk of developing atherosclerotic cardiovascular disease is well-established.Methods: Twenty-five pregnant women [19 with PE and 6 with normal pregnancy (NP)] were recruited during admission for delivery. HDL was isolated from blood samples. PON1 activity and HDL were analyzed. An in vitro model of endothelial cells was used to evaluate the effect of HDL on the transcription response of vascular cell adhesion molecule-1 (VCAM-1) and endothelial nitric oxide synthase (eNOS) mRNA expression.Results: PON1 activity (units/ml serum) was lower in the PE group compared to normal pregnancy (NP) (6.51 ± 0.73 vs. 9.98 ± 0.54; P = 0.015). Increased ApoA1 was released from PE-HDL as compared to NP-HDL (3.54 ± 0.72 vs. 0.89 ± 0.35; P = 0.01). PE-HDL exhibited increased VCAM-1 mRNA expression and decreased eNOS mRNA expression on TNF-α stimulated endothelial cells as compared to NP-HDL.Conclusions: HDL from women with PE reduced PON1 activity and increased ApoA1 release from HDL particles. This process was associated with increased HDL diameter, suggesting impaired HDL anti-oxidant activity. These changes might contribute to higher long-term cardiovascular risks among women with PE. [ABSTRACT FROM AUTHOR]

Endothelial cells (EC) and vascular smooth muscle cells (VSMC) are involved in the development of local and diffuse vasculopathies by participating in inflammatory processes that can lead to uncontrolled vascular complications. Our aim was to study the possible interactions of EC and VSMC in an in vitro coculture model exposed to diabetic-like conditions and the effect of vitamin D on cellular pathways that might lead to an inflammatory response. EC and VSMC were isolated from different umbilical cords and stimulated in an in vitro coculture model in a diabetic-like environment and calcitriol for 24 h. Total RNA and protein were extracted from cells and analyzed for the expression of selected inflammatory-related markers. The EC-VSMC coculture in a diabetic-like environment induced the expression of inflammatory markers such as Kruppel-like factors, thioredoxin-interacting protein (TXNIP), IL-6, and IL-8. Addition of vitamin D to the EC-VSMC coculture induced selective changes in the inflammatory response. This model could lead to a better understanding of the interactions between EC and VSMC in the inflammatory processes involved in diabetes and emphasizes the role of vitamin D in the inflammatory response. The use of different donors strengthens the significance of our findings showing that genetic variations do not affect the impact of vitamin D on the expression of inflammatory-related proteins in our model. [ABSTRACT FROM AUTHOR]