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Biomedical subjects

G Mozes

Publications and source records attributed to G Mozes.

At least 19 recordsLinked to original sources
PubMed2000

Thrombolysis for experimental deep venous thrombosis maintains valvular competence and vasoreactivity.

PURPOSE: Thrombolysis protects the structural and functional integrity of vein wall in an experimental model of acute deep venous thrombosis (DVT) immediately after treatment, but late sequelae have not been studied. We designed experiments to compare the effects of thrombolysis and surgical thrombectomy at 4 weeks after the treatment of DVT. METHODS: DVT was produced bilaterally in male mongrel dogs by proximal and distal femoral vein ligation. Five dogs underwent sham operation. After 48 hours, the ligatures were removed, and the thrombosis was treated with either Fogarty balloon catheter thrombectomy (shear force, 60 g; n = 6) or catheter-directed urokinase infusion (4000 U/min for 90 minutes; n = 6). At 4 weeks, patency and valvular competence were determined by duplex ultrasound scanning. Thrombogenicity was studied by the measurement of radiolabeled fibrin and platelet deposition. Veins were explanted and prepared for histologic examination, scanning electron microscopy, and functional studies in organ chambers. RESULTS: All veins were patent at 1 month. Recanalized thrombus was observed histologically in four (66%) thrombectomized veins, one (17%) thrombolyzed vein, and none of the sham-operated veins (P =.04). Scanning electron microscopy demonstrated similar luminal endothelial cell loss (11%-25%) in all three groups. Platelet and fibrin depositions were not different among groups. Valvular incompetence (reflux duration, >0.5 sec) did not differ significantly in the groups (thrombectomized veins, 2 of 12 (17%); thrombolyzed veins, 0 of 12 (0%); P = NS). In organ chamber studies, endothelium-dependent relaxations to calcium ionophore, but not adenosine diphosphate, were inhibited by an antagonist of nitric oxide production after thrombectomy (P <.05, thrombectomy vs sham- and thrombolysis-treated veins). All veins relaxed to exogenous nitric oxide. CONCLUSION: Both thrombectomy and thrombolysis restored patency and achieved similar valvular competence. Surgical thrombectomy, however, resulted in more residual thrombus and contributed to changes in endothelium-mediated relaxations at 4 weeks. Thrombolysis maintained both structural integrity and endothelial function.

Adenosine Diphosphate↗
PubMed2000

In vivo gene transfer of endothelial nitric oxide synthase to carotid arteries from hypercholesterolemic rabbits enhances endothelium-dependent relaxations.

BACKGROUND AND PURPOSE: Hypercholesterolemia is associated with abnormal endothelium-dependent vasorelaxation due to decreased nitric oxide bioavailability. Our aim was to examine the effect of adenovirus-mediated gene transfer of endothelial nitric oxide synthase (eNOS) to the hypercholesterolemic rabbit carotid artery in vivo. In addition, we examined whether adenovirus-mediated gene transfer was associated with vascular dysfunction. METHODS: Rabbits were fed a 1% cholesterol diet for 4 weeks followed by a 0.5% cholesterol diet for 6 weeks. Vascular reactivity was assessed in nontransduced carotid arteries from chow- and cholesterol-fed animals. In addition, carotid arteries were surgically isolated, and 2 separate doses of adenoviral vectors encoding eNOS or beta-galactosidase (AdbetaGal) on the contralateral side were delivered to the lumen (1x10(10) and 5x10(10) pfu/mL). RESULTS: Abnormal acetylcholine-mediated endothelium-dependent vasorelaxation was detected in the carotid artery from cholesterol-fed animals, whereas responses to calcium ionophore A23187 and diethylamine NONOate were normal. Vascular reactivity was similar in nontransduced and AdbetaGal-transduced hypercholesterolemic vessels. In vessels transduced with eNOS, transgene expression was demonstrated by immunostaining in both the endothelium and the adventitia and by Western blot analysis. High-dose but not low-dose eNOS gene transfer enhanced endothelium-dependent relaxation in vessels from cholesterol-fed rabbits. CONCLUSIONS: Adenovirus-mediated gene transfer of eNOS to carotid arteries of cholesterol-fed animals improves endothelium-dependent relaxation when an optimal viral titer is administered.

Animals↗
PubMed2000

Effects of laparoscopy on tumor growth.

Laparoscopic resections of colon cancer may affect survival. To address the effects of pneumoperitoneum on tumor cell biology, we developed an experimental model. Mice were injected with colonic tumor cells. Local and systemic effects of pneumoperitoneum were evaluated. Treated mice were randomly assigned to a control group, an open cecectomy group, or a laparoscopic-simulated cecectomy group. When a tumor inoculum was injected into the peritoneal cavity, the frequency of tumors was not significantly different for mice in the laparoscopic-simulated and open cecectomy groups (60% vs 62%, respectively). There was no significant difference in survival time between the laparoscopic-simulated and open cecectomy groups, with median survivals of 24 days versus 22 days, respectively. Finally, when tumor cells were injected subcutaneously, the frequency of tumor nodules and the size and weight of tumors were not different between the two surgical groups. Laparoscopic-simulated cecectomy does not appear to adversely effect local factors or favorably affect systemic factors influencing tumor growth or survival.

Adenocarcinoma↗
PubMed1999

The use of three-dimensional computed tomography in evaluating snapping scapula syndrome.

This article evaluates imaging of the scapula and scapulothoracic joint in patients with snapping scapula syndrome. Between 1990 and 1996, a total of 20 patients (10 men and 10 women) with snapping scapula syndrome were evaluated. Diagnosis was based on patient complaints and physical examination findings. There were 26 affected scapulae (6 patients had bilateral presentation). Imaging of the scapula included plain radiography, computed tomography (CT), and 3-dimensional computed tomography (3-D CT) reconstruction. Plain radiography revealed bony incongruity between the anterior aspect of the scapula and the chest wall in 7 scapulae, CT revealed such incongruity in 19 scapulae, and 3-D CT revealed incongruity in all 26 scapulae. Treatment was conservative, consisting of nonsteroidal anti-inflammatory drugs, a physiotherapy program, and subscapular injection of a local anesthetic and steroids. In 5 patients who responded poorly to conservative treatment, the region responsible for the snapping was resected. Pain relief and resolution of the snapping were complete following surgery in 4 patients, while pain and crepitation persisted in the fifth. Three-dimensional CT is recommended as the main imaging modality in the evaluation of any patient with snapping scapula syndrome who is a candidate for surgical intervention.

Adult↗
PubMed1998

Ex vivo gene transfer of endothelial nitric oxide synthase to atherosclerotic rabbit aortic rings improves relaxations to acetylcholine.

Cholesterol feeding results in impaired endothelium dependent vasorelaxation. The role of nitric oxide in this process is unclear. The aim of this study was to evaluate the role of nitric oxide in cholesterol-induced vasomotor dysfunction by examining the effect of overexpression of eNOS in the hypercholesterolemic rabbit aorta on vascular reactivity. Vascular rings from the thoracic aorta of hypercholesterolemic rabbits were exposed ex vivo either to an adenoviral vector encoding endothelial nitric oxide synthase (AdeNOS) or Escherichia coli beta Galactosidase (AdbetaGal). Transgene expression was examined by histochemistry for beta galactosidase, immunohistochemistry for eNOS and cyclic GMP measurements and vasomotor studies were performed. Transgene expression was found to localize to the endothelium and adventitia. cGMP levels were significantly greater in AdeNOS compared to AdbetaGal transduced rings. Acetylcholine mediated relaxation was significantly impaired in cholesterol fed rabbits and was markedly improved by overexpression of eNOS. These results suggest that reduced NO bioavailability observed in cholesterol-induced vascular dysfunction can be partially overcome by eNOS gene transfer.

Acetylcholine↗
PubMed1998

Effects of thrombolysis and venous thrombectomy on valvular competence, thrombogenicity, venous wall morphology, and function.

PURPOSE: The experiments were designed to compare the effects of thrombolytic therapy (TL) and balloon-catheter thrombectomy (TX) on valvular competence, thrombogenicity, venous wall morphology, and function after acute deep venous thrombosis (DVT) in canine veins. METHODS: The femoral veins of male mongrel dogs were ligated proximally and distally for 48 hours to induce DVT. The thrombosed veins were treated with either TL (n = 5) or TX (n = 9), or no treatment was rendered (n = 6). Sham-operated dogs were used as controls. TL was performed with catheter-directed infusion of urokinase at 4000 U/min for 90 minutes. Three hours after the treatment, the valvular competence was determined with duplex scanning, thrombogenicity determined with deposition of radio-labeled platelet and fibrin, and function determined with response to contractile and relaxing agonists in organ chambers. The structural integrity of the endothelial layer was assessed by means of scanning electron microscopy. RESULTS: The removal or lysis of the thrombus was successful in all cases. The valvular competence did not differ among the groups. The platelet deposition was the highest after TX (P <.05), and the fibrin deposition was not significantly different among the groups. In the organ chamber experiments, relaxations to adenosine diphosphate and nitric oxide were reduced after TX (P <.05). The contractions to serotonin were enhanced after TX. Scanning electron microscopy results showed a comparable (51% to 75%) endothelial loss with either treatment. CONCLUSIONS: After experimental acute DVT, the TL and the TX at 3 hours had similar effects on the valvular competence and the endothelial morphology. However, the TL reduced thrombogenicity, which is consistent with the preserved endothelial responses to platelet products. These data suggest that TL may preserve vein function after DVT and may reduce the long-term potential for recurrent DVT and post-thrombotic syndrome.

Animals↗
PubMed1998

Adenovirus-mediated gene transfer of macrophage colony stimulating factor to the arterial wall in vivo.

Macrophage colony stimulating factor (MCSF) is believed to play a key role in one of the earliest events in atherosclerosis, ie, monocyte to macrophage differentiation in the arterial intima. The aim of this study was to examine the biological effects of vascular wall expression of MCSF. A recombinant adenovirus vector encoding human MCSF (AdMCSF) was generated by standard techniques of homologous recombination in 293 cells. The rabbit carotid artery was transduced with AdMCSF. As negative controls, carotid arteries were transduced with either an adenoviral vector encoding beta-galactosidase, an adenoviral vector encoding apolipoprotein E, or diluent alone. Intima-media thickness ratio was calculated 5 and 21 days after transduction. The cell type present in intimal infiltrates was analyzed by immunohistochemistry. MCSF expression was demonstrated in the vessel wall of AdMCSF-transduced vessels by reverse transcription-polymerase chain reaction and immunofluorescence. In contrast to control vessels, adenovirus-mediated MCSF expression was associated with an intimal cellular infiltrate consisting of smooth muscle cells and small numbers of macrophages. Whereas the intima-media thickness ratio was greater in AdMCSF-transduced vessels at 5 days, this difference was no longer statistically significant at 21 days. These results suggest that MCSF may play a role in recruitment of monocytes and macrophages to the vessel wall and may contribute to smooth muscle cell proliferation and migration.

Adenoviridae↗
PubMed1998

Atherosclerosis in amputated legs of patients with and without diabetes mellitus.

BACKGROUND: The aim of this study was to compare the histomorphologic appearance of atherosclerosis in amputated legs of diabetic and non-diabetic patients. METHODS: Twenty-eight legs amputated below the knee for chronic ischaemia were studied. Fourteen legs were amputated in patients with diabetes (10 Type II, 4 nonclassified) and 14 in non-diabetics. The mean age of patients at the time of the amputation was 63.3 years in diabetics and 63.9 years in non-diabetics. Samples were taken from the main arteries at the following levels: the midleg, 5 cm above the ankle, 3 cm below the ankle and 10 cm below the ankle. Cross-sections of the arteries were examined with light microscopy and the severity of the occlusive disease determined using morphometric analysis. Medial calcification and chronic inflammation were assessed semiquantitatively. RESULTS: Arteries at 5 cm above the ankle were more severely stenotic in diabetics than in non-diabetics (p<0.05). In both diabetics and non-diabetics the posterior tibial and plantar arteries appeared to be the most stenotic. Medial calcification tended to be more prominent in diabetics than in non-diabetics. Chronic inflammation in the arterial wall occurred at the same degree in diabetics and non-diabetics. In non-diabetics chronic inflammation was more severe in the posterior tibial and plantar arteries than in the anterior tibial and dorsalis pedis arteries (p<0.04). Chronic arterial inflammation correlated with the severity of chronic arterial occlusive disease (p<0.0002). CONCLUSIONS: In diabetics occlusive disease in amputated legs is more severe in arteries above the ankle than in non-diabetics. However, no difference was demonstrated in this series in arteries of the ankle and foot. Diabetics are likely to have more medial calcification in the arteries than non-diabetics. Chronic inflammation in the arterial wall is associated with more severe stenosis.

Amputation, Surgical↗
PubMed1997

Adventitial gene transfer of recombinant endothelial nitric oxide synthase to rabbit carotid arteries alters vascular reactivity.

BACKGROUND: Adventitial gene transfer may serve as a tool to study vascular biology and may have therapeutic potential. We investigated the hypothesis that adenovirus-mediated transfer of the gene for endothelial nitric oxide synthase (eNOS) to the adventitia would alter vascular reactivity. METHODS AND RESULTS: Rabbit carotid arteries were surgically isolated and adenoviral vectors encoding eNOS (AdeNOS) or beta-galactosidase instilled into the periarterial sheath at a concentration of 1 x 10(10) pfu/mL. Arteries were harvested 4 days later for immunostaining, NOS enzymatic assay, measurement of cGMP, and vasomotor studies. Transgene expression in the adventitia was confirmed by histochemistry for beta-galactosidase and immunostaining for eNOS with a monoclonal antibody. Calcium-dependent NOS enzymatic activity and cGMP levels were significantly greater in the AdeNOS-transduced arteries. Maximal contractions to phenylephrine (10(-5) mol/L) were diminished in the AdeNOS-transduced arteries (4.6+/-0.2 versus 5.6+/-0.2 g; P<.05), but in the presence of the eNOS inhibitor N(G)-monomethyl-L-argininc (3x10(-4) mol/L) there was no difference between the two groups (7.1+/-0.2 versus 7.5+/-0.3 g; P=NS). Relaxations to calcium ionophore obtained during submaximal contractions to phenylephrine were significantly enhanced in the AdeNOS-transduced arteries (-log EC50, 7.77+/-0.08 versus 7.45+/-0.07; P<.02). CONCLUSIONS: We conclude that eNOS gene transfer to the adventitia alters vascular reactivity, as demonstrated by diminished contractile responses to phenylephrine and enhanced relaxations to calcium ionophore. This may represent a therapeutic strategy for vascular diseases characterized by decreased bioavailability of NO.

1-Methyl-3-isobutylxanthine↗
PubMed1997

Enhanced endothelium-dependent relaxations after gene transfer of recombinant endothelial nitric oxide synthase to rabbit carotid arteries.

We tested the effects of overexpression of the endothelial nitric oxide synthase (eNOS) gene in the normal arterial wall by adenoviral-mediated gene transfer. Rabbit carotid arteries were surgically isolated and exposed to adenoviral vectors encoding eNOS (AdeNOS) or beta-galactosidase (Ad betaGal) on the contralateral side. Vector solutions at a concentration of 1 x 10(10) plaque forming units/mL were instilled for 20 minutes before restoration of flow. Arteries were harvested 4 days later for immunostaining, measurement of cGMP, and vasomotor studies. Endothelium-specific gene transfer was confirmed by staining for beta-galactosidase in the Ad betaGal arteries. Immunostaining of en face endothelial cell imprints from AdeNOS-transduced arteries with a monoclonal antibody to eNOS showed increased immunoreactivity. Basal cGMP levels were significantly greater in the AdeNOS-transduced arteries (18.4+/-4.6 versus 4.2+/-0.5 pmol/mg protein; P<.05). Contractions to phenylephrine were significantly reduced in the AdeNOS-transduced arteries (area under curve, 106+/-5 versus 119+/-7; P<.05), but in the presence of the eNOS inhibitor, N(G)-monomethyl-L-arginine (L-NMMA, 3 x 10(-4) mol/L), there was no difference between the two (area under curve, 148+/-5 versus 153+/-6; P=NS). Relaxations to acetylcholine obtained during submaximal contractions to phenylephrine were significantly enhanced in the AdeNOS-transduced arteries (EC50, 7.45+/-0.05 versus 7.23+/-0.03; P<.05). We conclude that overexpression of eNOS in the endothelium results in diminished contractile responses, as well as enhanced endothelium-dependent relaxations. These findings imply a possible role for vascular eNOS gene transfer in the treatment of vasospasm and endothelial dysfunction.

Animals↗
PubMed1996

Effect of a femoral arteriovenous fistula on lower extremity venous hemodynamics after femorocaval reconstruction.

PURPOSE: To study the hemodynamic effects of an arteriovenous fistula (AVF) used as an adjunct to venous reconstructions and to determine the optimal size for such a fistula. METHODS: A model of limb circulation with an AVF (in vitro system) was constructed with silicon elastic tubes and 40% glycerin solution as the fluid medium. Pulsatile arterial flow and venous return was maintained with a roller pump and a centrifugal assist device. Flows and pressures were measured for three different fistula diameters (3, 4, and 5 mm). A canine model of venous hypertension with outflow obstruction was constructed in 15 adult mongrel dogs. After 7 to 13 days an externally supported 8-mm expanded polytetrafluoroethylene femorocaval graft was implanted with a distal AVF (3 mm, n = 5; 4 mm, n = 5; 5 mm, n = 5). Arterial and venous flows and venous pressures were measured proximal and distal to the fistula before and after exercise. RESULTS: In the in vitro system, flows through the venous graft increased with increasing fistula size, but venous return decreased progressively, increasing the distal venous pressure. In the canine model, flow in the venous graft increased with each AVF (p < 0.01). Only the 3-mm AVF resulted in decreased distal femoral vein pressure (p < 0.01), orthograde flow, and improved venous return with exercise. CONCLUSION: AVFs increased flow through the femorocaval grafts, yet they impeded venous return. The ideal AVF-to-graft ratio used in our study was 0.375, because it increased graft flow, permitted forward flow in the femoral vein while reducing pressure, and improved venous return with exercise.

Animals↗
PubMed1996

Surgical anatomy for endoscopic subfascial division of perforating veins.

PURPOSE: This study was undertaken to define the surgical anatomy of the medial perforating veins (PVs) of the leg and to provide information on how to gain access to all medial PVs from the superficial posterior compartment during a subfascial endoscopic procedure. METHODS: The venous anatomy of 40 limbs (from 23 cadavers) were studied. Medial PVs located between the ankle and the tibial tuberosity were dissected. None of the subjects had pathologic evidence of venous disease. Each PV's type (direct or indirect), size (< 1 mm, 1 to 2 mm, > 2 mm), location (distances from ankle [D1], and tibia [D2]), and accessibility from the superficial posterior compartment were recorded. RESULTS: Five hundred fifty-two PVs were identified (mean, 13.8; range, 7 to 22). Two hundred eighty-seven PVs (52%) directly connected the superficial with the deep systems, 228 (41%) were indirect muscle perforators, and 37 PVs (7%) were undetermined. One hundred thirty-seven PVs (25%) were > 2 mm. Sixty-three percent of PVs were accessible from the superficial posterior compartment. In the distal half of the leg, two groups of direct PVs could be identified (Cockett II: D1, 7 to 9 cm; Cockett III: D1, 10 to 12 cm). In the proximal half of the leg, paratibial direct PVs (D2 < or = 1 cm) were found clustered in three groups (D1, 18 to 22 cm; D1, 23 to 27 cm; D1, 28 to 32 cm). CONCLUSIONS: Our study confirmed the presence of the Cockett II and III PVs and three groups of proximal paratibial PVs, including the "24-cm" perforators. Two thirds of the medial direct PVs are accessible for endoscopic division from the superficial posterior compartment. To divide paratibial PVs, however, incision of the paratibial deep fascia is frequently required.

Cadaver↗
PubMed1991

Quadriparesis in the Laurence-Moon-Biedl-Bardet syndrome: case report.

A 36 year old patient known to suffer from the Laurence-Moon-Biedl-Bardet syndrome (LMBBS) developed spastic quadriparesis. The typical features of the syndrome, presented by this patient were polydactyly, obesity, hypogonadism, retinitis pigmentosa and relative mental retardation. Severe spinal cervical and lumbar canal stenosis imaged by plain X-rays and computerised tomography was found. Magnetic resonance imaging showed significant atrophy of the spinal cord, indicating that the cause of the quadriparesis was cervical myelopathy. The patient underwent laminoplasty with some improvement.

Adult↗
PubMed1990

Serum amyloid A, an acute phase protein, inhibits platelet activation.

The effect of serum amyloid A, an acute phase protein, on platelet function was studied. Serum amyloid A was isolated and purified from sera of patients with recent trauma. Serum amyloid A inhibited thrombin-induced gel-filtered platelet aggregation. However, it did not inhibit aggregation induced by collagen or adenosine diphosphate, nor did it influence the aggregation of platelet-rich plasma activated with thrombin. Further studies of its effect on thrombin-induced activities showed that serum amyloid A, at concentrations of 25 to 100 micrograms/ml (which are found in mild acute events), suppressed the increase of cytosolic [Ca2+], thromboxane generation, and carbon 14-labeled serotonin release in a dose-dependent fashion. Serum amyloid A did not interfere with the clotting or amidolytic activities of thrombin. Therefore, the data suggest a protective role for serum amyloid A in thromboembolic disease by specific interaction with thrombin-induced platelet activation. Amyloid A protein also markedly inhibited thrombin-induced platelet aggregation. Because amyloid A is homologous to the N-terminal portion of serum amyloid A, the observed activity probably resides in that part of the molecule. This finding may be of importance in localization of the active site on serum amyloid A.

Acute-Phase Proteins↗
PubMed1989

Serum amyloid A: an extremely sensitive marker for intensity of tissue damage in trauma patients and indicator of acute response in various diseases.

Acute response after traumatic events was studied in serial serum samples of 21 patients over a period of 13 days. Among the various biochemical and hematologic parameters, serum amyloid A (SAA) exhibited the most striking changes, with a pattern similar to that of the tissue marker creatine-P kinase (CPK). Maximal SAA level was detected 3-4 days after onset of the event, and reached 216 +/- 41 SEM gm/ml (normal range less than 2 gm/ml), while maximal CPK level was detected on the same day and reached 530 +/- 242 SEM IU/L (normal range 24-195 IU/L). Fibrinogen, leucocytes, platelets, albumin, alkaline phosphatase (AP), and calcium (Ca) each showed its own typical pattern of change. Fever did not develop. Comparison of SAA levels after various acute events suggests that damage to the myocardium is the most powerful stimulus for SAA induction, followed by traumatic events, arthritis, viral infections, and malignant diseases. It seems therefore that although acute response is considered a generalized reaction, it is not completely independent of the localized events which induce it. Among the known parameters, SAA is the most sensitive marker for monitoring the intensity of events.

Acute-Phase Proteins↗
PubMed1988

Congenital dislocation of the hip without acetabular dysplasia.

Congenital dislocation of the hip and acetabular dysplasia apparently are not constant features of the same disease. Cases of congenital dislocation of the hip with well-developed acetabula are reported periodically. The causative factors are genetically determined or unknown. In routine clinical work, a well-developed acetabulum improves the prognosis, even in the presence of severe dislocation. An acetabular operation is often unnecessary and the reduction is more stable. Once reduction is achieved, acetabular growth seems to continue at its usual pace in these patients.

Acetabulum↗