Effect of the Premature Infant Oral Motor Intervention on Sucking Capacity in Preterm Infants in Turkey: A Randomized Controlled Trial.

BACKGROUND: Preterm infants have oral feeding difficulty that often delays discharge, indicating a need for evidence-based interventions for oral-motor development. PURPOSE: To test the Premature Infant Oral Motor Intervention (PIOMI) on the development of oral-motor function, feeding, and anthropometric outcomes using sucking manometry. METHODS: A single-blind randomized experimental design was conducted with a sample of 60 preterm infants from 2 neonatal intensive care units between May 2019 and March 2020. The experimental group received PIOMI for 5 min/d for 14 consecutive days. Sucking capacity, anthropometrics (weight and head circumference), bottle feeding, breast/chest feeding initiation, and length of hospital stay were measured. The Yakut Sucking Manometer (PCT/TR2019/050678) was developed specifically for this study and tested for the first time. RESULTS: The experimental group had a statistically significant percent increase over controls in sucking power (69%), continuous sucking before releasing the bottle (16%), sucking time (13%), and sucking amount (12%) with partial η 2 values of interaction between the groups of 0.692, 0.164, 0.136, and 0.121, respectively. The experimental group had a higher increase in weight (89%) and head circumference (81%) over controls ( F = 485.130, P < .001; F = 254.754, P < .001, respectively). The experimental group transitioned to oral feeding 9.9 days earlier than controls ( t = -2.822; P = .007), started breast/chest feeding 10.8 days earlier ( t = 3.016; P = .004), and were discharged 3.0 days earlier. IMPLICATIONS FOR RESEARCH/PRACTICE: The PIOMI had a significant positive effect on anthropometrics, sucking capacity, readiness to initiate bottle and breast/chest feeding, and a 3-day reduction in length of hospital stay.

Analyses of soluble endoglin and matrix metalloproteinase 14 using enzyme-linked immunosorbent assay in the diagnosis and assessment of severity of early- and late-onset pre-eclampsia

Objective: Abnormal trophoblastic invasion and impaired placentation have a crucial role in the etiopathogenesis of preeclampsia (PrE). Trophoblastic cells are involved in invading the maternal decidua and remodelling of the spiral arteries with matrix metalloproteinase-14 (MMP-14). MMP-14 cleavage of endoglin releases its extracellular region, the soluble form of endoglin (s-ENG), into the maternal circulation. In PrE, there is a relationship between endothelial dysfunction and s-ENG concentration. The aim was to determine and compare the serum levels of s-ENG and MMP-14 in different groups of PrE patients and healthy subjects. Material and Methods: The study included 30 patients with late-onset preeclampsia (L-PrE) (group 1; gestational age ≥34 weeks), 33 patients with normal pregnancy (group 2; gestational age ≥34 weeks), 31 patients early-onset preeclampsia (E-PrE) (group 3; gestational age <34 weeks), and 31 patients with normal pregnancy (group 4; gestational age <34 weeks). s-ENG and MMP-14 concentrations measured using enzyme-linked immunosorbent assays were compared. Results: In all groups, MMP-14 concentrations decreased with increasing gestational age. s-ENG concentrations were highest in the E-PrE group. In groups 1 and 3, 29 had mild PrE while 32 suffered severe PrE and s-ENG concentrations did not differ between mild and severe preeclampsia (p=0.133). However, there was a significant difference in MMP-14 concentration comparing mild with severe PrE (3.11±0.61 vs 3.54±1.00; p=0.047, respectively). There was no correlation between s-ENG and MMP-14 concentrations. Conclusion: MMP-14 and s-ENG concentrations can be predictive biomarkers for the diagnosis of PrE. Maternal serum MMP-14 concentration may be a biomarker for determining the severity of PrE.

Maternal serum endothelial cell-specific molecule-1 level and its correlation with severity of early-onset preeclampsia.

Preeclampsia (PE), the primary pathology of which is endothelial cell (EC) dysfunction, has long-lasting effects such as cardiovascular disease. Therefore, it was decided to investigate the maternal serum concentrations of EC-specific molecule-1 in patients with early-onset preeclampsia (E-PE). This study was conducted on 33 pregnant women with E-PE and 35 healthy pregnant women matched for gestational age. EC-specific molecule-1 level was measured using a commercially available enzyme-linked immunosorbent assay kit. The mean EC-specific molecule-1 concentrations were not significantly different between the groups (651.7 ± 632.2 pg/mL vs. 425.9 ± 263.0 pg/mL, p=.056). Among women with E-PE, the median EC-specific molecule-1 concentration did not differ significantly by disease severity (p=.115). EC-specific molecule-1 is not involved in the pathogenesis of E-PE. However, some studies in the literature report that EC-specific molecule-1 concentrations increased during the diagnosis of PE. Therefore, well-designed studies with a large sample are needed in cases of E-PE.Impact StatementWhat is already known on this subject? There is an increased risk of cardiovascular disease (CVD) in early-onset preeclampsia (E-PE) which is linked with endothelial dysfunction. Endothelial cell (EC)-specific molecule-1 stands out as an important marker in EC dysfunction related conditions such as preeclampsia.What the results of this study add? This study showed that EC-specific molecule-1 is not associated with the CVDs risk linked with endothelial dysfunction in E-PE. Additionally, there was also no significant relationship was detected between the severity of E-PE and EC-specific molecule-1 concentrations.What the implications are of these findings for clinical practice and/or further research? Endothelial cell-specific molecule-1 is not involved in the pathogenesis of E-PE. Moreover, advantageous and easy-to-measure markers are needed in larger sample studies to better understand the aetiology of E-PE.

Hypobaric-hypoxia-induced pulmonary damage in rats ameliorated by antioxidant erdosteine.

Free radical-mediated injury to lung and pulmonary vasculature is an important mechanism in hypoxia-induced lung damage. In this study, we aimed to investigate the potential protective effects of erdosteine as an antioxidant agent on hypobaric hypoxia-induced pulmonary hypertension. Adult male rats were assigned randomly to three groups. The first group of rats was exposed to hypobaric-hypoxia and the second group was treated with erdosteine (20mg/kg, daily) for 2 weeks, during which time they were in a hypoxic chamber. These groups were compared with normoxic controls. All rats were sacrificed after 2 weeks. The hypoxia-induced increase in right ventricle to left ventricle plus septum weight ratio (from 0.20+/-0.01 to 0.26+/-0.01) was reduced significantly in the erdosteine-treated group (0.23+/-0.01). Malondialdehyde levels were elevated (from 0.33+/-0.11 to 0.59+/-0.02) and total antioxidant status was not changed significantly (from 1.77+/-0.42 to 2.61+/-0.23) by hypoxia. In contrast to the hypoxia-exposed group, malondialdehyde levels were significantly decreased in the erdosteine-treated group (0.37+/-0.02). Total antioxidant status (4.03+/-0.22) was significantly higher in erdosteine-treated rats when compared to non-treated rats. Histopathological examination demonstrated that erdosteine prevented inflammation and protected lung parenchyma and pulmonary endothelium of hypoxia-exposed rats.

The effect of different dialysis membranes on oxidative stress and selenium status.

BACKGROUND: Oxidative stress is an important risk factor for the development and progression of several complications in hemodialysis patients. The aim of this study was to evaluate the effects of two different dialysis membranes on oxidative stress and selenium status. METHODS: Forty long-term dialysis patients and 20 age-matched healthy controls were enrolled into our study. Serum malondialdehyde (MDA) and selenium (Se) concentrations, and glutathione peroxidase (GSH-Px) activities were determined before and after hemodialysis (HD) using a hemophan (H) or a polysulfone (PS) membrane. RESULTS: MDA levels in the HD patients were significantly higher than those in the control group (p < 0.001). GSH-Px activity and selenium concentrations were significantly lower in HD patients compared to the control group (p < 0.001). MDA levels were significantly increased (p < 0.05); GSH-Px activity and selenium concentrations were significantly reduced (p < 0.001) in the PS membrane group compared to H membrane group after HD. CONCLUSIONS: Comparing with H membrane, PS membrane caused more oxidative stress and lower levels of Se in HD patients.