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John Hess

Publications and source records attributed to John Hess.

At least 55 records · Page 3Linked to original sources
PubMed2004

Rac regulates thrombin-induced tissue factor expression in pulmonary artery smooth muscle cells involving the nuclear factor-kappaB pathway.

Pulmonary hypertension is associated with enhanced thrombogenicity of the vessel wall contributing to vascular remodeling. However, the signaling mechanisms promoting this prothrombotic state are not resolved. Here we investigated the role of the GTPase Rac in the regulation of tissue factor (TF) expression and activity in response to thrombin in pulmonary artery smooth muscle cells (PASMC). TF mRNA and protein expression and surface procoagulant activity were increased by thrombin in PASMC. These responses were enhanced in the presence of the constitutively active Rac mutant RacG12V, but were abrogated in cells expressing dominant-negative RacT17N. Thrombin and RacG12V also increased human TF promoter activity primarily involving a sequence between -636 and -111 bp containing a distal, nuclear factor-kappaB (NFkappaB)-dependent enhancer element. Indeed, thrombin and RacG12V stimulated NFkappaB-dependent transcriptional activity, and overexpression of p50/p65 significantly increased human TF promoter activity. Moreover, in RacG12V-overexpressing cells, TF promoter activity was significantly decreased by coexpression of dominant-negative mutants of IkappaBalpha and IkappaBKalpha, which prevent NFkappaB activation. As enhanced NFkappaB activity has been observed in patients with pulmonary hypertension, Rac-dependent activation of the NFkappaB pathway may be a critical element promoting thrombin-induced TF expression and activity, and thus a prothrombotic state in pulmonary hypertension.

Cells, Cultured↗
PubMed2004

Characterization of a mutation in the lens-specific CP49 in the 129 strain of mouse.

PURPOSE: The 129 strain of mouse carries a mutation in the gene for CP49 (phakinin), an intermediate filament protein thus far demonstrated only in the lens fiber cell. As such, these mice represent naturally occurring mutants of interest in the study of the lens cytoskeleton. However, this strain of mouse is also widely used as a source of embryonic stem cells in gene-targeting studies. The presence of a mutation in a lens-specific gene can confound interpretation of studies in which lens genes have been knocked out. In the present study, both the genotype and phenotype of these mice were characterized, to permit an evaluation of the biological impact of this mutation and to facilitate the discrimination between wild-type and mutant animals that have been derived from this strain in gene-targeting studies. METHODS: The CP49 cDNA and, when relevant, the genomic DNA sequences were determined for the 129/SvJ and C57BL/6J mice and from a commercially available 129/OLa P1 genomic clone. PCR primers were screened for their capacity to discriminate between the mutant and wild-type CP49 genes. Northern blot analysis was used to assess mRNA levels for CP49, filensin, and gammaS-crystallin (control). Western blot analysis was used to identify changes in protein size and abundance. The impact of the mutation on lens architecture was evaluated at the light-microscope level. Lens fiber cell ghosts from mutant and wild-type mice were examined in the electron microscope for the presence of beaded filaments. Lens clarity was assessed by slit lamp. RESULTS: The 129 strain of mice exhibited a 6303-bp deletion from the end of intron B, and the beginning of exon 2. This deletion results in the loss of the exon 2 splice acceptor site, absence of exon 2 from the CP49 mRNA, and dramatically reduced levels of CP49 mRNA. The CP49 protein was undetectable by Western blot analysis. Messenger RNA levels for filensin, CP49's assembly partner, were normal, but protein levels were sharply reduced. Light microscopy established that the initial differentiation and elongation of the fiber cells proceeded normally. Electron microscopy showed the absence of beaded filaments, whereas slit lamp microscopy showed a slowly emerging and progressive loss of optical clarity. CONCLUSIONS: The 129/SvJ and 129/OLa strains of mice harbor a mutation that sharply reduces CP49 mRNA levels and essentially eliminates both CP49 and the beaded filament. These lenses exhibited a slow but progressive loss of optical clarity with age. Thus, the 129 strain of mouse behaves as a functional CP49 knockout. The loss of clarity in the lenses of these animals and the absence of beaded filaments (and any attendant interactions that may exist between beaded filaments and other lens proteins/structures) suggest that gene-targeting studies of lens proteins in which the 129 strain was used as a source of embryonic stem cells may need reevaluation.

Amino Acid Sequence↗
PubMed2004

Follow-up of adults with coarctation of the aorta: comparison of helical CT and MRI, and impact on assessing diameter changes.

OBJECTIVES: To compare images of the aorta obtained with helical CT (HCT) scanning and MRI for the follow-up of adults with coarctation of the aorta (CoA). DESIGN: Longitudinal study. SETTING: Department of adult congenital heart disease in a tertiary university hospital. PATIENTS: A total of 37 adults (age range, 16 to 68 years; women, 13) with CoA (after surgery, 34 patients; native, 2 patients; after balloon-angioplasty, 1 patient) MEASUREMENTS AND RESULTS: All patients underwent both HCT and MRI of the thoracic aorta within a mean (+/- SD) time interval of 1.86 +/- 1.11 years. Aortic diameters measured at six intrathoracic levels showed a high correlation (r = 0.79 to 0.94). On average, slightly lower diameters were measured with MRI (1.2 mm). But there was a substantial variation between the two measurements with differences of up to 9 mm. All other pathomorphologic abnormalities were detected and classified similarly with both methods. CONCLUSIONS: HCT and MRI are similarly useful for the noninvasive evaluation of the thoracic aorta in patients with CoA. But there can be a substantial variation in two subsequent measurements without an overall substantial bias toward larger diameter in one of the two methods. In repetitive studies, changes of the diameters should be interpreted with care, especially when assessing the progression of aortic diameters.

Adolescent↗
PubMed2003

Hearts late after fontan operation have normal mass, normal volume, and reduced systolic function: a magnetic resonance imaging study.

OBJECTIVES: The purpose of this study was to assess ventricular mass, volume, and systolic function in patients late after Fontan operation by cardiac magnetic resonance imaging. BACKGROUND: An assessment of determinants for ventricular function in post-Fontan patients was intended. METHODS: Twenty-three unselected patients (9 female, 14 male) at a median age of 19.4 years (range, 7.8 to 31.3 years), at a median time of 10.5 years (range, 4.1 to 18 years) after Fontan operation were studied. A standard 1.5-T scanner was used, and analysis was performed using dedicated software. Ten healthy volunteers (median age 26.4, range 18 to 39.3 years) served as the control group. RESULTS: Median end-systolic mass index was 72.2 g/m(2) (range, 43 to 138 g/m(2)) and 86.6 g/m(2) (range, 52 to 123 g/m(2)) in the control group (p = NS). Median end-diastolic ventricular volume was 64 ml/m(2) (range, 32 to 117 ml/m(2)) compared with 67.7 ml/m(2) (range, 59 to 75 ml/m(2)) in the control group (p = NS). Median ejection fraction was 49.3% (range, 20% to 63%) compared with 64.8% (range, 57% to 79%) in normals (p = 0.00001). CONCLUSIONS: We conclude that long-term survivors of a Fontan operation have normal ventricular mass, normal volume, but reduced systolic ventricular function.

Adolescent↗
PubMed2003

Intramyocardial synthesis of pro- and anti-inflammatory cytokines in infants with congenital cardiac defects.

OBJECTIVES: We sought to test the hypothesis that cytokines would be expressed in the myocardium of infants with congenital cardiac defects and to identify the signaling pathways involved. BACKGROUND: Mechanical stress upregulates pro-inflammatory cytokines in the myocardium. METHODS: Fifteen infants with tetralogy of Fallot (TOF) (n = 7) or with ventricular septal defects (VSDs) (n = 8) were investigated. Concentrations of pro- and anti-inflammatory cytokines and of the inducible nitric oxide synthase (iNOS) were measured by enzyme-linked immunosorbent assay and/or Western blotting in the right ventricular myocardium taken during cardiac surgery. Activation of the nuclear factor-kappa-B (NF-kappa-B) and p38 mitogen-activated protein kinase (MAPK) pathways was assessed by electrophoretic mobility shift assay with supershift and/or Western blotting, respectively. RESULTS: The pro-inflammatory cytokines tumor necrosis factor (TNF)-alpha, interleukin (IL)-1-beta, and IL-6 and the anti-inflammatory cytokine IL-10 were detected in the myocardium of all patients. Concentrations of the pro-inflammatory cytokines and also of phosphorylated p38 MAPK were higher in patients with TOF than in those with VSD and correlated with the degree of pressure overload of the right ventricle. Levels of phosphorylated I-kappa-B-alpha, iNOS, and IL-10 were similar in patients with TOF and in those with VSD. CONCLUSIONS: Our results show intramyocardial synthesis of pro-inflammatory cytokines in infants with congenital cardiac defects. This is associated with activation of both the NF-kappa-B and p38 MAPK pathways. The latter could be particularly important for the transduction of mechanical signals in the infant's myocardium. Synthesis of IL-10 indicates an intramyocardial anti-inflammatory potential in this age group.

Cytokines↗
PubMed2003

Protein-losing enteropathy in patients with Fontan circulation: is it triggered by infection?

INTRODUCTION: Protein-losing enteropathy (PLE) is a recognised complication of the Fontan circulation. Its pathogenesis is not fully understood, however, and it is unclear why its onset occurs months or even years after Fontan surgery. PATIENTS: We report a 4.5-year-old girl with Fontan circulation who developed PLE almost 1 year after surgery. At the time of onset the patient had rotavirus enteritis and streptococcal tonsillitis. We have reviewed the records of seven other patients with longstanding PLE. In six of these patients we identified infections at the onset of symptoms. None of our patients had evidence of opportunistic infection. DISCUSSION AND CONCLUSION: The immune system of patients with PLE is compromised, but reports on recurrent opportunistic infections are rare. The present observations suggest that infection and inflammation may be associated with the onset of PLE. The mechanism of how infection may trigger PLE warrants further investigation.

Child↗
PubMed2003

Emergency hospital admissions and three-year survival of adults with and without cardiovascular surgery for congenital cardiac disease.

OBJECTIVE: This study determined the quantity and nature of emergencies leading to unscheduled hospital admissions of adults with congenital cardiac disease and their mid-term survival. RESULTS: During 1 year, 429 adults with congenital cardiac diseases were admitted 571 times, and 124 admissions (22%) of 95 patients (22%) were emergency admissions. Fifteen of the 95 patients were seen for the first time in 1 of the participating centers. The underlying anomalies were Fallot's tetralogy and pulmonary atresia (n = 26/7), univentricular heart after Fontan procedure (n = 25), atrial septal defect (n = 18), Eisenmenger syndrome (n = 12), complete transposition (n = 11), and others (n = 25). Indications for admission were cardiovascular complications (n = 103; 83%) (arrhythmia, cardiac failure, syncope, pacemaker problems, pericardial tamponade, and sudden death), infections (n = 8, 6%) (endocarditis, pacemaker infection, pneumonia, and cerebral abscess), acute chest pain (n = 7; 6%), and acute abdominal pain (n = 4; 3%). All patients required immediate emergency care, and 16 patients (17%) required urgent cardiovascular or abdominal surgery. Six patients died during the hospital stay. During a follow-up of 2.9 years (SD 0.8), 16 (18%) of the discharged patients died, and 2 additional patients underwent heart or heart-lung transplantation. CONCLUSION: Adults with congenital cardiac disease often experience serious emergency situations with a high in-hospital and mid-term post-hospital mortality. Care given by physicians with special expertise is important in this specific group of patients.

Adolescent↗
PubMed2003

Pulmonary blood pressure, not flow, is associated with net endothelin-1 production in the lungs of patients with congenital heart disease and normal pulmonary vascular resistance.

OBJECTIVE: Endothelin-1 concentrations are increased in patients with increased mean pulmonary arterial pressure, pulmonary blood flow, and pulmonary vascular resistance. However, endothelin-1 concentrations have not been well characterized in patients with congenital heart disease and normal pulmonary vascular resistance. In particular, it is unclear whether pressure or flow is the key regulator of endothelin- 1 in this setting. We tested the hypothesis that pulmonary blood pressure and not flow is associated with net endothelin-1 production in patients with congenital heart disease and normal pulmonary vascular resistance. METHODS: With a commercially available immunoassay, we measured endothelin-1 concentrations in pulmonary arterial and pulmonary venous plasma of 56 consecutive patients with congenital heart disease and pulmonary vascular resistance less than 2 U. m(2) undergoing cardiac catheterization. We used multiple linear regression to analyze the effect of demographic and hemodynamic variables on pulmonary arterial and venous endothelin-1 concentrations and on the change of endothelin-1 concentration over the pulmonary vascular bed. RESULTS: Multiple linear regression revealed that of all the hemodynamic variables tested, mean pulmonary arterial pressure had the greatest effect on increasing the change of endothelin-1 concentration over the pulmonary vascular bed (P <.0001). Pulmonary blood flow did not have any effect on endothelin-1 concentrations or on the change of endothelin-1 concentration over the pulmonary vascular bed. CONCLUSIONS: This study shows that pulmonary blood pressure and not flow is associated with net endothelin-1 production in patients with congenital heart disease and normal pulmonary vascular resistance.

Blood Pressure↗
PubMed2003

Delineation of intra-atrial reentrant tachycardia circuits after mustard operation for transposition of the great arteries using biatrial electroanatomic mapping and entrainment mapping.

INTRODUCTION: Intra-atrial reentrant tachycardia (IART) circuits after Mustard operation remain incompletely understood due to the complex atrial anatomy after extensive surgical procedures. The aim of this study was to delineate IART circuits and their relations to the individual anatomic boundaries in Mustard patients. METHODS AND RESULTS: Twelve patients (10 men and 2 women; age 29 +/- 4.6 years) with atrial tachyarrhythmias after Mustard operation were included in this study. During 14 IARTs and 2 focal atrial tachycardias, electroanatomic mapping and entrainment mapping were performed in both the systemic venous atrium and the pulmonary venous atrium. The latter was accessed via a retrograde transaortic approach. Thirteen IARTs used a single-loop reentrant circuit, and 1 IART used a dual-loop reentrant circuit. Ten (77%) of 13 single-loop reentrant circuits used the tricuspid annulus (TA) as their central barrier. The remaining 3 IARTs rotated around the inferior vena cava (IVC) (n = 2) or ostium of the right upper pulmonary vein (n = 1). In 6 (60%) of the 10 peritricuspid IARTs, both pulmonary venous atrium and systemic venous atrium components of the mid-portion of the TA-IVC isthmus were demonstrated to be part of the reentry. Overall, 12 (86%) of 14 IARTs in 10 patients were successfully ablated by bridging two barriers that constrained the reentrant circuit. Eight (80%) of 10 peritricuspid circuits were abolished by linear ablation connecting the TA to the IVC (n = 4), incisional scar (n = 2), patch (n = 1), and atriotomy (n = 1). CONCLUSIONS: In Mustard patients, the TA serves as the most frequent central barrier of IART. Biatrial electroanatomic mapping combined with entrainment mapping facilitates delineation of IART circuits in relation to their anatomic barriers and enables the design of individual ablation strategies to achieve high success.

Adult↗
PubMed2003

Intrahepatic synthesis of tumor necrosis factor-alpha related to cardiac surgery is inhibited by interleukin-10 via the Janus kinase (Jak)/signal transducers and activator of transcription (STAT) pathway.

SUMMARY: OBJECTIVES To identify the signaling pathways involved in the anti-inflammatory shift of the cytokine balance due to hypothermia during cardiopulmonary bypass. DESIGN Experimental animal study. SETTING Department of experimental surgery of a university hospital. SUBJECTS Young pigs. INTERVENTIONS Animals underwent normothermic (37 degrees C) or hypothermic (28 degrees C) cardiopulmonary bypass (n = 6 each). Samples of liver tissue were taken before and 6 hrs after cardiopulmonary bypass. MEASUREMENTS AND MAIN RESULTS Intrahepatic expression of tumor necrosis factor-alpha, interleukin-10, inducible nitric oxide synthase, and suppressor of cytokine signaling-3 was detected by reverse transcriptase polymerase chain reaction and/or Western blotting. Concentrations of the inhibitory protein of nuclear factor-kappaB, IkappaB, and of the signal transducer and activator of transcription (STAT)-3 were measured by Western blotting. The DNA-binding activity of nuclear factor-kappaB and STAT-3 was assessed by electrophoretic mobility shift and supershift assays. Liver cell necrosis and apoptosis were assessed by histology and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling assay, respectively. Pigs operated on in hypothermia showed significantly higher intrahepatic concentrations of interleukin-10 and lower concentrations of tumor necrosis factor-alpha than the others. They also showed a lower percentage of hepatic cell necrosis but not of apoptosis. This anti-inflammatory reaction observed in the hypothermic group was associated with a higher expression of suppressor of cytokine signaling-3 and with increased activation of STAT-3. Activation of nuclear factor-kappaB and expression of inducible nitric oxide synthase, however, were not significantly different between both groups. CONCLUSION Our results show that hypothermia during cardiopulmonary bypass up-regulates interleukin-10 via STAT-3 activation, which in turn leads to the attenuation of tumor necrosis factor-alpha expression and to hepatic protection.

Animals↗
PubMed2003

Targeted deletion of the lens fiber cell-specific intermediate filament protein filensin.

PURPOSE: To determine the function of the lens fiber cell-specific cytoskeletal protein, filensin, in lens biology. METHODS: Targeted genomic deletion was used to delete exon 1 and the transcriptional start site of the filensin gene. Resultant chimeric animals were bred to homozygosity for the mutant allele. These animals were outbred to mice bearing the wild-type CP49 alleles to eliminate the mutant CP49 gene carried by the 129 strain of mice. Animals homozygous for the mutated filensin gene and wild-type CP49 gene were compared with wild-type and heterozygous animals by Northern and Western blot analyses, light and electron microscopy, and slit lamp microscopy. RESULTS: Disruption of the filensin gene successfully blocked production of filensin mRNA, reduced levels of filensin's assembly partner CP49, and prevented the assembly of beaded filaments. Despite the absence of beaded filaments, lenses did not show obvious changes in fetal development, nor in the differentiation of epithelial cells into mature fiber cells, as judged by light microscopic analysis. Filensin knockouts began to show evidence of light-scattering by 2 months and worsened with age. Heterozygous animals exhibited an intermediate phenotype, showing a reduction in filensin transcript and moderate light-scattering at 5 months. CONCLUSIONS: The lens fiber cell-specific intermediate filament protein filensin is essential for beaded filament assembly. However, although beaded filaments are not needed for normal lens fetal development or fiber cell differentiation, they appear to be necessary for the long-term maintenance of optical clarity. The mechanism by which the absence of filensin and the beaded filament affects optical clarity has yet to be defined.

Animals↗
PubMed2002

More accurate quantification of pulmonary blood flow by magnetic resonance imaging than by lung perfusion scintigraphy in patients with fontan circulation.

BACKGROUND: Quantitative evaluation of pulmonary perfusion using lung perfusion scintigraphy in patients with atriopulmonary anastomosis (APA) or total cavopulmonary connection (TCPC) or partial cavopulmonary connection (PCPC) is difficult because of preferential draining of the venae cavae to one lung. Scintigraphy is the gold standard. Phase-velocity MRI (PV-MRI) is a new technique for determining pulmonary perfusion. The aim of this study was therefore to determine whether PV-MRI is more accurate than scintigraphy for quantitative evaluation of pulmonary perfusion ratios in patients with APA, TCPC, or PCPC. METHODS AND RESULTS: We studied 15 patients with APA, TCPC, or PCPC (16+/-7 years old, 4 female). Twelve patients (15+/-8 years old, 3 female) with a single pulmonary blood source supplied by a subpulmonary ventricle, ensuring complete mixing of the radioactive tracer before entering the pulmonary circulation, served as controls. Pulmonary scintigraphy and PV-MRI were performed in all patients. Bland-Altman analysis showed a clinically unacceptable difference of 7.1% right pulmonary blood flow (27.2% upper and -13.0% lower limit of agreement) between the two methods in the study group. The two methods agreed excellently in the control group (difference, 1.6%; 4.0% upper and -7.2% lower limit of agreement), showing that the bad agreement in the study group was caused by the problems encountered using pulmonary scintigraphy in patients with APA, TCPC, or PCPC. CONCLUSIONS: Because of preferential caval flow into either lung, PV-MRI is more accurate for evaluating pulmonary perfusion ratios than lung perfusion scintigraphy in patients with Fontan-like circulation.

Adolescent↗
PubMed2002

NADPH oxidase mediates tissue factor-dependent surface procoagulant activity by thrombin in human vascular smooth muscle cells.

BACKGROUND: Tissue factor (TF) initiates the extrinsic coagulation cascade leading to thrombin formation. Thrombin induces TF mRNA in vascular smooth muscle cells (VSMCs), thereby contributing to the prolonged procoagulant activity and enhanced thrombogenicity at sites of vascular injury. However, the signaling mechanisms mediating this thrombogenic cycle are unclear. Characteristically, vascular injury promotes the generation of reactive oxygen species (ROS). Because ROS exert signaling functions, we investigated whether the NADPH oxidase, an important source of ROS in VSMCs, contributes to upregulation of TF by thrombin. METHODS AND RESULTS: Thrombin not only stimulated TF mRNA expression, but also TF-dependent surface procoagulant activity in cultured human VSMCs. This response was attenuated by antioxidants; the flavin inhibitor diphenylene-iodonium, Clostridium difficile toxin B, which inhibits Rho GTPases, p22phox antisense oligonucleotides, or the dominant-negative RacT17N mutant. Inhibitors of p38 MAP kinase and phosphatidylinositol (PI) 3-kinase also prevented thrombin-stimulated TF mRNA expression. Furthermore, thrombin stimulated the phosphorylation of the PI 3-kinase target protein kinase B/Akt in a redox-sensitive and NADPH oxidase-dependent manner. CONCLUSION: These findings indicate that the NADPH oxidase is essentially involved in the redox-sensitive induction of TF mRNA expression and surface procoagulant activity by thrombin. This response is mediated by NADPH oxidase-dependent activation of p38 MAP kinase and the PI 3-kinase/protein kinase B/Akt pathway. Given that active TF promotes thrombin formation, the NADPH oxidase may play a crucial role in perpetuating the thrombogenic cycle in the injured vessel wall.

Bacterial Proteins↗
PubMed2002

Does age at the time of elective cardiac surgery or catheter intervention in children influence the longitudinal development of psychological distress and styles of coping of parents?

AIMS: To assess the influence of age at a cardiac procedure of children, who underwent elective cardiac surgery or interventional cardiac catheterisation for treatment of congenital cardiac defects between 3 months and 7 years of age, on the longitudinal development of psychological distress and styles of coping of their parents. METHODS: We used the General Health Questionnaire to measure psychological distress, and the Utrecht Coping List to measure styles of coping. Parents completed questionnaires on average respectively 5 weeks prior to, and 18.7 months after, cardiac surgery or catheter intervention for their child. RESULTS: Apart from one exception, no significant influence was found of the age at which children underwent elective cardiac surgery or catheter intervention on the pre- to postprocedural course of psychological distress and the styles of coping of their parents. Across time, parents of children undergoing surgery reported, on average, significantly higher levels of psychological distress than parents of children who underwent catheter intervention. After the procedure, parents of children who underwent either procedure reported significantly lower levels of psychological distress, and showed a weaker tendency to use several styles of coping, than did their reference groups. CONCLUSION: Age of the children at the time of elective cardiac surgery or catheter intervention did not influence the course of psychological distress of their parents, nor the styles of coping used by the parents. Future research should investigate in what way the age at which these cardiac procedures are performed influences the emotional and cognitive development of the children.

Adaptation, Psychological↗
PubMed2002

Diameters of the thoracic aorta throughout life as measured with helical computed tomography.

OBJECTIVE: The use of helical computed tomography is well established in the evaluation of the thoracic aorta. Nevertheless, normal diameters and their changes during adult life according to this method are not available. We planned to set up normal diameters for the thoracic aorta of adults obtained by helical computed tomography. METHODS: Seventy adults, 17 to 89 years old, without any signs of cardiovascular disease were investigated with helical computed tomography. Aortic diameters were measured at seven predefined thoracic levels. RESULTS: Aortic diameters (mean +/- SD) were 2.98 +/- 0.46 cm at the aortic valve sinus, 3.09 +/- 0.41 cm at the ascending aorta, 2.94 +/- 0.42 cm proximal to the innominate artery, 2.77 +/- 0.37 cm at the proximal transverse arch, 2.61 +/- 0.41 cm at the distal transverse arch, 2.47 +/- 0.40 cm at the isthmus, and 2.43 +/- 0.35 cm at the diaphragm. Men had slightly longer diameters than did women. All diameters increased with age. There was no influence of weight, height, or body surface area. After normalization to the diameter at diaphragmatic level, no statistically significantly influential factor could be detected. CONCLUSIONS: This study delineates normal intrathoracic aortic diameters for helical computed tomography, including relationships with sex and age. Pathologic dimensions of the aorta should preferably be provided as percentiles or z scores.

Adolescent↗
PubMed2002

Redox signaling through NADPH oxidases: involvement in vascular proliferation and coagulation.

Reactive oxygen species (ROS) have been shown to play important functions as signaling molecules in the vasculature. Several NADPH oxidase isoforms have been identified in endothelial and smooth muscle cells, which are largely responsible for basal and stimulated ROS production in these cells. Moreover, evidence increases that activation of these enzymes contributes to stimulation of signaling cascades modulating essential functions in the vasculature such as endothelial and smooth muscle cell proliferation as well as thrombosis.

Animals↗