Comparison of the superb microvascular imaging technique and the color Doppler techniques for evaluating children's testicular blood flow.

OBJECTIVE: We have compared conventional Color Doppler (CD) and Power Doppler (PD) techniques, which are used for evaluating the testicular blood flow in small children, and the Superb Microvascular Imaging (SMI), which is a new technique. We have also investigated their contributions to testicular evaluations. PATIENTS AND METHODS: We evaluated blood flow in testicles using a grading system with CD, PD and SMI techniques. We determined the average duration of the three techniques. RESULTS: There was a statistically significant difference between the SMI and CD techniques for all patients (p < 0.001, p = 0.001). When we compared the PD and SMI, either as much or more vascular information was obtained (p = 0.106). There was a statistically significant difference between the application durations of the tests (p < 0.05). CONCLUSIONS: Superb Microvascular Imaging yields more detailed vascular information in blood flow in testicles in small children, than either CD or PD. Furthermore, this technique decreases the duration of the examination at a significant level. Superb Microvascular Imaging may represent an alternative method that can be used safely for evaluating blood flow in the testicles of small children. Additional studies may increase the reliability of SMI.

Polyorchidism and adenomatous hyperplasia of the rete testis: a case report with sonographic and magnetic resonance imaging findings and review of literature.

Supernumerary testis or polyorchidism is a rare congenital anomaly with about 200 reported cases in the literature. It may be associated with cryptorchidism, testicular torsion and neoplasms. Ultrasonography and magnetic resonance imaging are effective noninvasive methods of accurately detecting polyorchidism. In most cases, ultrasonography is diagnostic and magnetic resonance imaging plays confirmatory role by providing additional information if complicated with neoplasia. We report a case of 16-year-old man with right supernumerary testis associated with adenomatous hyperplasia of the rete testis, its sonographic and magnetic resonance imaging findings and management.

Can biliary-cyst communication be predicted by Gd-EOB-DTPA-enhanced MR cholangiography before treatment for hepatic hydatid disease?

AIM: To evaluate the role of gadolinium ethoxybenzyl diethylenetriamine pentaacetic acid (Gd-EOB-DTPA)-enhanced magnetic resonance cholangiography (MRC) in the evaluation of biliary-cyst communication (BCC) before treatment for hepatic hydatid disease (HHD). MATERIAL AND METHODS: Thirty-one patients with clinical and laboratory follow-up for HHD with suspected diagnosis of BCC underwent three-dimensional (3D) T2-weighted MRC and T1-weighted contrast-enhanced MRC, dynamic 3D gradient echo (GRE) sequences, using Gd-EOB-DTPA to identify the presence or absence of BCC. A total of 45 hepatic hydatid cysts in the 31 patients were evaluated for cyst diameter, BCC, and the time to contrast-enhancement of the hydatid cyst after Gd-EOB-DTPA injection. The surgical and interventional radiological procedures and imaging findings were compared. The sensitivity, specificity, and accuracy of both techniques in identification of BCC were calculated. RESULTS: The accuracy of contrast-enhanced MRC for identifying BCC was superior with a sensitivity of 87.4% and accuracy of 90.5% (p < 0.05). A diameter of ≥10 cm was associated with significantly increased risk of BCC on contrast-enhanced MRC images (p < 0.05). CONCLUSION: The use of Gd-EOB-DTPA-enhanced MRC yields information that complements T2-weighted MRC findings and improves identification of BCC. The use of T2-weighted MRC, in addition to contrast-enhanced MRC, is recommended to increase preoperative accuracy of identifying BCC.

The utility of multidetector computed tomography for evaluation of congenital heart disease.

BACKGROUND: Congenital heart diseases (CHD) are the leading cause of birth defect-related deaths. Multi detector computed tomography (MDCT) plays an important role for imaging CHD in addition to echocardiography and provides a comprehensive evaluation of complex heart malformations for the referring cardiologist. The aim of the study was to evaluate the utility of MDCT in the assessment of CHD. MATERIALS AND METHODS: A 102 patients with CHD were investigated after initial assessment by echocardiography. The information obtained by MDCT and findings of echocardiography were reviewed together by paediatric cardiologists and cardiac radiologists. Perioperative anatomic descriptions, wherever available(n = 34) formed the gold standard for the comparison. RESULTS: The clinical consensus diagnosis defined 154 cardiovascular lesions in the patients. The results were classified in groups. We present the appearance of various congenital cardiac lesions seen in clinical practice. CONCLUSIONS: MDCT provides important information about anatomic details of CHD for the referring cardiologist. The evaluation of different anatomic structures such as heart, great vessels, lungs and abdomen is possible in one acquisition with this technique.

Hyperglycaemia promotes cerebral barrier dysfunction through activation of protein kinase C-ß.

AIM: To examine whether protein kinase C (PKC) and associated downstream mechanisms are involved in hyperglycaemia (HG)-evoked blood-brain barrier (BBB) damage. METHODS: The activities of total PKC (Peptag assay), NADPH oxidase (lucigenin assay) and matrix metalloproteinase-2 (MMP-2; gelatin zymography) were measured in human brain microvascular endothelial cells (HBMEC) exposed to normoglycaemia (5.5 mM) or HG (25 mM) using the specific assays indicated in parentheses. The integrity and function of the in vitro models of human BBB were assessed by measurements of transendothelial electrical resistance and paracellular flux of permeability markers, respectively. Occludin protein expression was studied by immunoblotting. RESULTS: HG significantly compromised the BBB integrity and enhanced total PKC activity to which increases in PKC-ß and PKC-ßII isoforms contributed the most. Elevations in NADPH oxidase and MMP-2 activities and decreases in occludin levels contributed to barrier dysfunction. Selective inhibition of PKC-ß isoform prevented the changes observed in occludin expression and the aforementioned enzyme activities and thus effectively preserved barrier integrity. Similarly, apocynin, a specific NADPH oxidase inhibitor, also effectively neutralized the effects of HG on barrier integrity, MMP-2 activity, occludin expression and PKC-ß activity. CONCLUSION: HG promotes cerebral-barrier dysfunction through activation of PKC-ß and consequent stimulations of oxidative stress and tight junction dissolution.

Partial anomalous pulmonary venous return associated with vascular anomalies of the aorta: multidetector computed tomography findings.

Partial anomalous pulmonary venous return (PAPVR) is a congenital anomaly that involves drainage of one to three pulmonary veins directly into the right heart or systemic venous system, creating a partial left-to-right shunt. This drainage is associated with cardiac abnormalities such as mitral stenosis and pulmonary stenosis, patent ductus arteriosus, and atrial septal defects. We report a case of PAPVR associated with vascular anomalies of the aorta by multidetector computed tomography in an adult female patient.

Subvalvular membrane on the left ventricular outflow tract: multidetector computerised tomography imaging.

In this report, we describe a patient with a subvalvular membrane on the left ventricular outflow tract. Discrete subvalvular membrane is a cause of left ventricular outflow tract narrowing. Multidetector computerised tomography can demonstrate the anatomical three-dimensional view of this region and guide for surgery.

Oxidative stress and its role in the pathogenesis of ischaemic stroke.

Stroke is one of the leading causes of mortality and morbidity, with astronomical financial repercussions on health systems worldwide. Ischaemic stroke accounts for approximately 80-85% of all cases and is characterised by the disruption of cerebral blood flow and lack of oxygen to the affected area. Oxidative stress culminates due to an imbalance between pro-oxidants and antioxidants and consequent excessive production of reactive oxygen species. Reactive oxygen species are biphasic, playing a role in normal physiological processes and are also implicated in a number of disease processes, whereby they mediate damage to cell structures, including lipids, membranes, proteins, and DNA. The cerebral vasculature is a major target of oxidative stress playing a critical role in the pathogenesis of ischaemic brain injury following a cerebrovascular attack. Superoxide, the primary reactive oxygen species, and its derivatives have been shown to cause vasodilatation via the opening of potassium channels and altered vascular reactivity, breakdown of the blood-brain barrier and focal destructive lesions in animal models of ischaemic stroke. However, reactive oxygen species are involved in normal physiological processes including cell signalling, induction of mitogenesis, and immune defence. Primarily, this review will focus on the cellular and vascular aspects of reactive oxygen and nitrogen species generation and their role in the pathogenesis of ischaemia-reperfusion phenomena. Secondly, the proposed mechanisms of oxidative stress-related neuronal death will be reflected upon and in summation specific targeted neuroprotective therapies targetting oxidative stress and their role in the pathogenesis of stroke will be discussed.

Antioxidants attenuate hyperglycaemia-mediated brain endothelial cell dysfunction and blood-brain barrier hyperpermeability.

AIMS: Hyperglycaemia (HG), in stroke patients, is associated with worse neurological outcome by compromising endothelial cell function and the blood-brain barrier (BBB) integrity. We have studied the contribution of HG-mediated generation of oxidative stress to these pathologies and examined whether antioxidants as well as normalization of glucose levels following hyperglycaemic insult reverse these phenomena. METHODS: Human brain microvascular endothelial cell (HBMEC) and human astrocyte co-cultures were used to simulate the human BBB. The integrity of the BBB was measured by transendothelial electrical resistance using STX electrodes and an EVOM resistance meter, while enzyme activities were measured by specific spectrophotometric assays. RESULTS: After 5 days of hyperglycaemic insult, there was a significant increase in BBB permeability that was reversed by glucose normalization. Co-treatment of cells with HG and a number of antioxidants including vitamin C, free radical scavengers and antioxidant enzymes including catalase and superoxide dismutase mimetics attenuated the detrimental effects of HG. Inhibition of p38 mitogen-activated protein kinase (p38MAPK) and protein kinase C but not phosphoinositide 3 kinase (PI3 kinase) also reversed HG-induced BBB hyperpermeability. In HBMEC, HG enhanced pro-oxidant (NAD(P)H oxidase) enzyme activity and expression that were normalized by reverting to normoglycaemia. CONCLUSIONS: HG impairs brain microvascular endothelial function through involvements of oxidative stress and several signal transduction pathways.

Smoking impairs endothelial function in human saphenous vein in an ex vivo model.

The aim of this ex vivo experimental study was to assess the effect of smoking, diabetes mellitus, and hypertension on endothelial function in human saphenous vein, a commonly used conduit for coronary and peripheral arterial bypass surgery. A segment of long saphenous vein harvested during infrainguinal bypass surgery was mounted in an organ bath for isometric tension studies. Vein rings were precontracted to submaximal contraction with phenylephrine, followed by endothelium-dependent relaxation with acetylcholine. Long saphenous vein segments were collected from 26 patients, including five females, with a mean age of 66.4 years (range 48-92). Current smokers had impaired endothelium-dependent relaxation compared to ex- and nonsmokers (10.2%, n=13, vs. 32.9%, n=13; p<0.010). However, ex-smokers and nonsmokers did not have a significant difference in relaxant responses to acetylcholine (29.1%, n=8, vs. 24.6%, n=5; p=nonsignificant [ns]). Similarly, diabetic and nondiabetic patients did not show a significant difference in endothelium-dependent relaxation (23.1%, n=10, vs. 15.6%, n=16; p=ns). The relaxant responses in hypertensive and normotensive patients were not different (20.4%, n=12, vs. 22.5%, n=14; p=ns). Smoking has a deleterious effect on the endothelial function of saphenous vein, and smoking cessation may improve the long-term durability of saphenous vein used as a bypass graft in patients undergoing arterial reconstruction.

Carotid intima-media thickness: is it correlated with stroke side?

OBJECTIVE: The objective of the present study was to investigate the possible correlation between the common carotid artery (CCA) intima-media thickness (IMT) and the infarct side. METHOD: The CCA IMTs in patients with atherosclerotic non-lacunar stroke were measured. RESULTS: The mean age of the patients was 64.3 +/- 10.7 years (range 40-83 years) and 42 of 100 patients were male. The infarcts were at the left side in 53 patients and at the right side in 47 patients. The mean CCA IMT was 1.02 +/- 0.18 mm at the infarct side and 0.87 +/- 0.17 mm at the contralateral side. The difference between them was statistically significant (P < 0.01). Although the mean age of the patients with a left-sided infarct was greater than that of the patients with a right-sided infarct, the difference was not statistically significant. CONCLUSION: Our results suggest that CCA IMT may be used in prediction of possible infarct side, and in the prediction of potential risk of stroke by evaluating the IMT of both CCAs separately.

High glucose mediates pro-oxidant and antioxidant enzyme activities in coronary endothelial cells.

AIM: Excess levels of free radicals such as nitric oxide (NO) and superoxide anion (O(2)(-)) are associated with the pathogenesis of endothelial cell dysfunction in diabetes mellitus. This study was designed to investigate the underlying causes of oxidative stress in coronary microvascular endothelial cells (CMECs) exposed to hyperglycaemia. METHODS: CMECs were cultured under normal (5.5 mmol/l) or high glucose (22 mmol/l) concentrations for 7 days. The activity and expression (protein level) of endothelial NO synthase (eNOS), inducible NOS (iNOS), NAD(p)H oxidase and antioxidant enzymes, namely, superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx) were investigated by specific activity assays and Western analyses, respectively, while the effects of hyperglycaemia on nitrite and O(2)(-) generation were investigated by Griess reaction and cytochrome C reduction assay, respectively. RESULTS: Hyperglycaemia did not alter eNOS or iNOS protein expressions and overall nitrite generation, an index of NO production. However, it significantly reduced the levels of intracellular antioxidant glutathione by 50% (p < 0.05) and increased the protein expressions and activities of p22-phox, a membrane-bound component of pro-oxidant NAD(p)H oxidase and antioxidant enzymes (p < 0.05). Free radical scavengers, namely, Tiron and mercaptopropionylglycine (MPG) (0.1-1 micromol/l) reduced hyperglycaemia-induced antioxidant enzyme activity and increased glutathione and nitrite generation to the levels observed in CMEC cultured in normoglycaemic medium (p < 0.01). The differences in enzyme activity and expressions were independent of the increased osmolarity generated by high glucose levels as investigated by using equimolar concentrations of mannitol in parallel experiments. CONCLUSIONS: These results suggest that hyperglycaemia-induced oxidative stress may arise in CMEC as a result of enhanced pro-oxidant enzyme activity and diminished generation of antioxidant glutathione. By increasing the antioxidant enzyme capacity, CMEC may protect themselves against free radical-induced cell damage in diabetic conditions.

Antioxidant vitamins C and E ameliorate hyperglycaemia-induced oxidative stress in coronary endothelial cells.

OBJECTIVE: Vitamins C and E have protective features in many disease states associated with enhanced oxidative stress. The aim of this study was to investigate whether vitamin(s) C and/or E modulate hyperglycaemia-induced oxidative stress by regulating enzymatic activities of prooxidant, i.e. NAD(P)H oxidase and/or antioxidant enzymes, namely endothelial nitric oxide synthase (eNOS), superoxide dismutase, catalase and glutathione peroxidase, using coronary microvascular endothelial cells (CMEC). METHODS: CMEC were cultured under normal (5.5 mM) or high glucose (22 mM) concentrations for 7 days. The enzyme activities were determined by specific assays. The levels of O(2) (-) and nitrite were measured by cytochrome c reduction and Griess assays respectively. RESULTS: Hyperglycaemia did not alter eNOS activity or overall nitrite generation, an index of NO production. However, it increased NAD(P)H oxidase and antioxidant enzyme activities (p < 0.05). Specific inhibitors of NAD(P)H oxidase, i.e. phenylarsine oxide (0.1-3 microm) and 4-(2-aminoethyl)benzenesulfonyl fluoride (5-100 microm) and vitamins C and E (0.1-1 microm) significantly reduced prooxidant and antioxidant enzyme activities in CMEC exposed to hyperglycaemia (p < 0.01). The differences in enzyme activities were independent of increases in osmolarity generated by high glucose levels as investigated by using equimolar concentrations of mannitol in parallel experiments. CONCLUSIONS: Vitamins C and E may protect CMEC against hyperglycaemia-induced oxidative stress by concomitantly regulating prooxidant and antioxidant enzyme activities.

Investigation of the C242T polymorphism of NAD(P)H oxidase p22 phox gene and ischaemic heart disease using family-based association methods.

Ischaemic heart disease is a complex phenotype arising from the interaction of genetic and environmental factors. Excessive production of reactive oxygen species leading to endothelial dysfunction is believed to be important in the pathogenesis of ischaemic heart disease. The NAD(P)H oxidase system generates superoxide anions in vascular cells; however, the role of the C242T polymorphism of the NAD(P)H oxidase p22 phox gene in ischaemic heart disease is unclear due to contradictory results from case-control studies. Consequently, we applied family-based association tests to investigate the role of this polymorphism in ischaemic heart disease in a well-defined Irish population. A total of 1023 individuals from 388 families (discordant sibships and parent/child trios) were recruited. Linkage disequilibrium between the polymorphism and ischaemic heart disease was tested using the combined transmission disequilibrium test (TDT)/sib-TDT (cTDT) and pedigree disequilibrium test (PDT). Both cTDT and PDT analyses found no statistically significant excess transmission of either allele to affected individuals (P =0.30 and P =0.28, respectively). Using robust family-based association tests specifically designed for the study of complex diseases, we found no evidence that the C242T polymorphism of the p22 phox gene has a significant role in the development of ischaemic heart disease in our population.