Preliminary study showing the relationship between platelet fibronectin, sialic acid, and ADP-induced aggregation levels in coronary heart disease.

Several studies indicate that thrombosis plays an important role in the pathogenesis of coronary heart disease (CHD). Fibronectin is a multifunctional protein in plasma, other body fluids, and cell surface and plays an important role in platelet functions, including mediation of cell-cell and cell-surface interactions. Sialic acid is a regular constituent of glycoproteins and gangliozides in the outer cell membrane of mammalian cells. Therefore, the sialic acid content of platelets, which are characterized by their ability to aggregate with each other, can be important in leading to thrombus formation. In this study, platelet fibronectin, sialic acid-, and adenosine diphosphate (ADP)-induced platelet aggregation levels were determined in patients with CHD. Platelet sialic acid concentrations were determined by Warren's method. Platelet aggregation tests with ADP in platelet-rich plasma (PRP) were analyzed by use of an aggregometer. Platelet homogenate fibronectin levels were determined by ELISA. Total protein levels were determined by Lowry method. Our results indicate that, in patients with no vessel disease (patients with no obstructed vessel but suffering from chest pain, like angina pectoris) platelet fibronectin levels were significantly lower than the total of the other patients (patients with 1, 2, or 3 obstructed coronary vessels) (p<0.05). Sialic acid levels in patients with no vessel disease were significantly lower than the total of the patient group (p<0.05). There was significant (+) correlation between platelet aggregation, platelet fibronectin, platelet sialic acid, and severity of disease (p<0.05). Our preliminary findings suggest that, especially platelet fibronectin levels potentially represent a pathogenic factor for CHD.     

Detection of inadvertent catheter movement into a pulmonary vein during radiofrequency catheter ablation by real-time impedance monitoring

Introduction: During radiofrequency ablation to encircle or isolate the pulmonary veins (PVs), applications of radiofrequency energy within a PV may result in stenosis. The aim of this study was to determine whether monitoring of real-time impedance facilitates detection of inadvertent catheter movement into a PV.
Methods and Results: In 30 consecutive patients (mean age 53 ± 11 years) who underwent a left atrial ablation procedure, the three-dimensional geometry of the left atrium, the PVs, and their ostia were reconstructed using an electroanatomic mapping system. The PV ostia were identified based on venography, changes in electrogram morphology, and manual and fluoroscopic feedback as the catheter was withdrawn from the PV into the left atrium. Real-time impedance was measured at the ostium, inside the PV at approximately 1 and 3 cm from the ostium, in the left atrial appendage, and at the posterior left atrial wall. There was an impedance gradient from the distal PV (127 ± 30 Ω) to the proximal PV (108 ± 15 Ω) to the ostium (98 ± 11 Ω) in each PV (P < 0.01). There was no significant impedance difference between the ostial and left atrial sites. During applications of radiofrequency energy, movement of the ablation catheter into a PV was accurately detected in 80% of the cases (20) when there was an abrupt increase of ≥4 Ω in real-time impedance.
Conclusion: There is a significant impedance gradient from the distal PV to the left atrium. Continuous monitoring of the real-time impedance facilitates detection of inadvertent catheter movement into a PV during applications of radiofrequency energy. (J Cardiovasc Electrophysiol, Vol. 15, pp. 1-5, June 2004)     

Four years' experience with the Edwards-Tekna bileaflet valve prosthesis

BACKGROUND AND AIM OF THE STUDY: Although over 20,000 Edwards-Duromedics valves were implanted worldwide between 1982 and May 1988, use of the valve was voluntarily suspended by the manufacturer in May 1988 on the basis of reported leaflet escapes. In 1990, a modified version was introduced to the market, the Edwards-Tekna. The study aim was to evaluate the short-term outcome with this revised valve. METHODS: Between 1994 and 1998, 137 patients (67 males, 70 females; mean age 36.3+/-9.1 years) underwent heart valve replacement with the Edwards-Tekna prosthesis. Among these patients, 72 had isolated mitral valve replacement, 59 isolated aortic valve replacement, and six double-valve replacement. RESULTS: Early hospital mortality was 0.72% (n = 1). Follow up was 95% complete (129/136 patients discharged from hospital). Mean follow up was 24.9+/-10.5 months (range: 2 to 48 months); total follow up was 282.9 patient-years (pt-yr). Actuarial freedom from complications at two-year follow up and linearized incidence (%/pt-yr) of these events were: late mortality 87.8+/-8.5% (1.77%/pt-yr); thromboembolism 89.8+/-4.9% (2.12%/pt-yr); anticoagulation-related bleeding 97.8+/-1.5% (0.71%/pt-yr); prosthetic valve endocarditis 99.1+/-0.9% (0.35%/pt-yr); valve-related mortality 98.2+/-1.2% (0.71%/pt-yr); and valve-related morbidity and mortality 85.0+/-5.0% (4.24%/pt-yr). There was no structural valve failure such as leaflet escape in this series. Clinically significant hemolysis was not encountered (mean postoperative plasma LDH level 345+/-124 IU/l). Preoperatively, 69% of patients were in NYHA classes III/IV; at two years postoperatively 90% of survivors were in classes I/II. CONCLUSION: The Edwards-Tekna mechanical valve prosthesis has shown excellent overall clinical performance in the short term, though long-term data are needed to confirm its durability.     

HLA-DR B1 and DQ B1 polymorphisms in patients with coronary artery ectasia

OBJECTIVES: The purpose of our study was to evaluate the significance of polymorphisms in HLA class II genes in coronary artery ectasia (CAE) patients. METHODS AND RESULTS: Twenty-six patients with CAE without associated cardiac defects were enrolled in the study. CAE was defined as luminal dilation of 1.5- to 2.0-fold of normal limits. Ninety-five healthy subjects who were donors for different organ transplantations, were chosen as control group. Physical examination, electrocardiography and chest X-ray were completely normal in these cases. Both the patients and the control group were screened and compared for their HLA class II genotypes. HLA-DR B1*13, DR16, DQ2 and DQ5 genotypes were significantly more frequent in the patient group.When the known risk factors of coronary heart disease were compared in the patients carrying these genotypes with the non-carrying group, no significant differences were encountered. CONCLUSIONS: HLA-DR B1*13, DR16, DQ2 and DQ5 may be associated with the pathogenesis and increase the risk of CAE.     

Effect of smoking on neonatal and maternal serum and breast milk leptin levels

Maternal smoking is considered to be a risk factor for low birth weight. It is hypothesized that alteration in leptin concentration may be associated with reduced fetal growth. In this study, we assess the effect of smoking during pregnancy on maternal and neonatal serum leptin concentrations, and also on breast milk leptin levels. When the infants were brought to routine physical examination at 7 days old, blood samples and breast milk specimens were taken for leptin measurement from mothers who smoked during pregnancy and their newborns. Nonsmoking mothers and their infants were recruited randomly over the same period as a control group. Maternal age, number of pregnancy, weight of the mothers, birth weight, and gestational age of the infants were similar in both groups (p > 0.05). There was no significant difference between groups in maternal serum and breast milk leptin levels (p = 0.14 and p = 0.96, respectively). However, serum leptin levels were found significantly lower in neonates born to smoking mothers compared with infants born to nonsmoking mothers (p = 0.02). Our findings suggest that maternal smoking dose not have an effect on maternal serum and breast milk leptin levels but decreases neonatal serum leptin concentration independent of birth weight.     

Prevalence of tuberculosis infection and its relationship to stunting in children (under five years) household contact with new tuberculosis cases

BackgroundChildren who inhabit the same house with tuberculosis (TB) patients are at high risk for infection and illness with TB. Nutritional status (stunting) in children is related to the child's ability to withstand MTB (Mycobacterium Tuberculosis). This study aims to estimated the prevalence of tuberculosis infection and its relationship to stunting in children (under five years) with household contact (HHC) with new TB cases.MethodsA cross-sectional design was implemented. Conducted in July 2018–April 2019 at 13 Public Health Center in Makassar City. The sample size was calculated using one sample situation-about precision formula. Samples were children under five who had contact with new diagnosed TB cases. Tuberculosis infection was measured by TST (tuberculin skin test). Logistic regression with causal model to examine TB infection relationship with stunting and covariate variable, analyzed using Stata/MP 13.0 software.ResultsOne hundred twenty-six (126) eligible children. Prevalence of tuberculosis infection was 38.10%. Frequency of stunted was 31 children (24.60%). Stunted nutritional status (aPR): 2.36, 95% CI 1.60–3.44), boys (aPR: 1.47, 95% CI 0.96–2.25), not getting BCG immunization (aPR: 1.58, 95%) CI 0.89–2.82), and high contact intensity (aPR: 2.62, 95% CI 1.10–6.22) best predicted the tuberculosis infection in children with TB case household contacts with a model contribution of 64%.ConclusionStunted nutritional status (moderate and severe), boys, not getting BCG immunization, and high contact intensity are the determinants of TB infection transmission in children HHC with TB. Children under five years of age who have close contact with TB cases should be targeted for priority interventions to prevent the transmission of TB infection and progressing to TB cases.     

Evaluation of hydrogen peroxide-assisted endoscopic ultrasonography-guided necrosectomy in walled-off pancreatic necrosis: A single-center experience

Hydrogen peroxide is a liquid that functions in mechanical removal of the necrotic tissue via the elimination of tissue debris.In this study, we aimed to evaluate the effectiveness of the use of hydrogen peroxide in necrosectomy treatment of walled-off pancreatic necrosis.Records of 24 patients who were diagnosed with pancreatic necrosis or walled-off pancreatic necrosis and underwent endoscopic necrosectomy (EN) were retrospectively assessed. Patients were divided into 2 groups; hydrogen peroxide used for treatment or not used, and these 2 groups were compared.A total of 24 patients underwent endoscopic intervention for walled-off pancreatic necrosis. Procedural success was comparable between the 2 groups. During the post-procedural follow-up, the duration of the hospital stay, recurrence, and complication rates were found to be similar in both groups. The mean number of the endoscopic interventions was significantly lower in the hydrogen peroxide group (4.2 ± 1.4 vs 6.1 ± 4.2; P = .01).The use of hydrogen peroxide for EN in walled-off pancreatic necrosis patients seems to have similar efficiency and safety. However, it can be said that the use of hydrogen peroxide could reduce the number of endoscopic procedures.     

Acetaminophen toxicity up-regulates MRP2 expression in the liver of cats: an old story with new vision

This study was conducted to clarify the role of efflux transporter MRP₂ in acetaminophen-induced hepatotoxicity in cats. Sixteen mixed bred male cats and four liver samples from mixed breed male dogs were used. The cats were assigned into four groups (n?=?4), received saline and 2, 10 and 50?mg/kg doses of acetaminophen orally for 14 days. Unlike the intact dogs, the MRP₂ was not detectable in control cats. MRP₂ at mRNA level was expressed in the liver of cats, which received the medium and high doses. Data suggest that the MRP₂ expression may involve in the acetaminophen-induced hepatotoxicity in cats.     

A rare cause of hydrops fetalis in two Gaucher disease type 2 patients with a novel mutation

Metabolic Brain Disease - Gaucher disease type 2 is the most progressive and the rarest form of Gaucher disease, defined as the acute neuronopathic type. We presented two GD2 patients who died...     

The efficiency of Poly(ADP‐Ribose) Polymerase (PARP) cleavage on detection of apoptosis in an experimental model of testicular torsion

The aim of this study was to evaluate the histopathological and apoptotic changes occurring in the rat ipsilateral and contralateral testes, after experimental spermatic cord torsion, and to explore and the role of poly(ADP‐ribose) polymerase (PARP) cleavage in testicular torsion–detorsion injury. A total of 37 Wistar albino rats were subjected to 720° unilateral spermatic cord torsion for 1, 2 and 4 h, followed by 4‐h reperfusion, or else to a sham operation (control group). Histology of the testicle was evaluated using haematoxylin–eosin (H&E) staining and Johnsen's scoring system. Germ cell apoptosis was evaluated via active caspase‐3 immunostaining, and PARP expression levels were evaluated via Western blotting. The mean Johnsen's tubular biopsy scores (JTBS) of the ipsilateral testicles were lower for all torsion groups than for the controls (P < 0.05), but the JTBS of the contralateral testicles were only lower in the 4‐h torsion group (P < 0.05). The mean apoptosis score (AS) of the ipsilateral and contralateral testicles was significantly higher in the torsion groups than in the sham group. AS increased correlatively with torsion time, in both testicles. The effect of testicular torsion on PARP cleavage was time dependent, with the highest effect observed after 4 h of testicular torsion (P < 0.05). Testicular torsion caused time‐dependent histological changes, apoptosis and increases in PARP cleavage. Our results suggest that testicular torsion–detorsion injury caused cell damage and germ cell apoptosis that apparently involved cleavage of PARP. Increased PARP cleavage could, in turn, lead to enhanced apoptosis.