Lower leg and foot contributions to turnout in female pre-professional dancers: A 3D kinematic analysis.

Turnout is a central element of classical ballet which involves sustained external rotation of the lower limbs during dance movements. Lower leg and foot compensation mechanisms which are often used to increase turnout have been attributed to the high incidence of lower limb injury in dancers. Evaluation of dancers' leg posture is needed to provide insight into the lower limb kinematic strategies used to achieve turnout. The primary purpose of this study was to use 3D kinematic analyses to determine the lower leg and foot compensations that are incorporated by female university dancers to accentuate their turnout. Active and passive external tibiofemoral rotation (TFR) was also measured. A moderate-strong negative relationship was observed between hip external rotation (HER) and foot abduction in the three first position conditions. A moderate negative relationship was found between passive TFR and foot abduction in all first position conditions. Our findings suggest dancers are more likely to pronate, than rotate the knee to compensate for limited HER. Dancers with a limited capacity to pronate may force additional rotation via the knee. Ongoing research would benefit from more in-depth analyses of the foot/ankle complex using a multi-segment foot model.

An exploratory, open-label, randomized, multicenter study to investigate the pharmacodynamics of a glycoengineered antibody (imgatuzumab) and cetuximab in patients with operable head and neck squamous cell carcinoma.

BACKGROUND: In addition to inhibiting epidermal growth factor receptor (EGFR) signaling, anti-EGFR antibodies of the IgG1 'subtype' can induce a complementary therapeutic effect through the induction of antibody-dependent cell-mediated cytotoxicity (ADCC). Glycoengineering of therapeutic antibodies increases the affinity for the Fc-gamma receptor, thereby enhancing ADCC. PATIENTS AND METHODS: We investigated the changes in immune effector cells and EGFR pathway biomarkers in 44 patients with operable, advanced stage head and neck squamous cell carcinoma treated with two preoperative doses of either glycoengineered imgatuzumab (GA201; 700 or 1400 mg) or cetuximab (standard dosing) in a neoadjuvant setting with paired pre- and post-treatment tumor biopsies. RESULTS: Significant antitumor activity was observed with both antibodies after just two infusions. Metabolic responses were seen in 23 (59.0%) patients overall. One imgatuzumab-treated patient (700 mg) achieved a 'pathological' complete response. An immediate and sustained decrease in peripheral natural killer cells was consistently observed with the first imgatuzumab infusion but not with cetuximab. The functionality of the remaining peripheral natural killer cells was maintained. Similarly, a pronounced increase in circulating cytokines was seen following the first infusion of imgatuzumab but not cetuximab. Overall, tumor-infiltrating CD3+ cell counts increased following treatment with both antibodies. A significant increase from baseline in CD3+/perforin+ cytotoxic T cells occurred only in the 700-mg imgatuzumab group (median 95% increase, P < 0.05). The most prominent decrease of EGFR-expressing cells was recorded after treatment with imgatuzumab (700 mg, -34.6%; 1400 mg, -41.8%). The post-treatment inflammatory tumor microenvironment was strongly related to baseline tumor-infiltrating immune cell density, and baseline levels of EGFR and pERK in tumor cells most strongly predicted therapeutic response. CONCLUSIONS: These pharmacodynamic observations and relationship with efficacy are consistent with the proposed mode of action of imgatuzumab combining efficient EGFR pathway inhibition with ADCC-related immune antitumor effects. CLINICAL TRIAL REGISTRATION NUMBER: NCT01046266 (ClinicalTrials.gov).

Single-leg squats can predict leg alignment in dancers performing ballet movements in "turnout".

The physical assessments used in dance injury surveillance programs are often adapted from the sports and exercise domain. Bespoke physical assessments may be required for dance, particularly when ballet movements involve "turning out" or external rotation of the legs beyond that typically used in sports. This study evaluated the ability of the traditional single-leg squat to predict the leg alignment of dancers performing ballet movements with turnout. Three-dimensional kinematic data of dancers performing the single-leg squat and five ballet movements were recorded and analyzed. Reduction of the three-dimensional data into a one-dimensional variable incorporating the ankle, knee, and hip joint center positions provided the strongest predictive model between the single-leg squat and the ballet movements. The single-leg squat can predict leg alignment in dancers performing ballet movements, even in "turned out" postures. Clinicians should pay careful attention to observational positioning and rating criteria when assessing dancers performing the single-leg squat.

Improvement of endocardial and vascular endothelial function on myocardial performance by captopril treatment in postinfarct rat hearts.

Background-Endocardial (EE) and myocardial capillary vascular endothelial (myocap VE) cells have been shown to modulate the contractile characteristics of myocardium in a calcium-dependent manner. We evaluated the endothelial-myocardial interaction in the rat postinfarction myocardial infarction (MI) model and the effects of captopril. Methods and Results-Wistar rats were divided into 4 groups treated for 4 weeks: (1) control; (2) infarcted controls (left anterior coronary artery ligation); (3) infarcted+captopril 2 g/L in drinking water; and (4) infarct+captopril+triton intracoronary injection. Coronary VE function was evaluated by infusion of serotonin in Langendorff preparations (n=31), and the myocardial contractile characteristics were investigated by use of isolated papillary muscles (n=44). Cardiac mRNA for endothelial constitutive nitric oxide synthase (ecNOS) was measured, and its cellular location was evaluated by immunohistochemistry. Serotonin-induced increase in coronary flow was decreased in infarct controls compared with controls (4.6% versus 53.4%, P<0.01) but not in the 2 infarct+captopril groups. Intracoronary triton injection decreased serotonin-induced coronary flow in the infarct+captopril+triton group. All MI groups had decreased total tension in isolated papillary muscles. EE removal by triton immersion decreased total tension in all groups except for infarct controls (3.3 versus 3.2 g/mm(2)). Cardiac ecNOS mRNA decreased in the control infarct group but remained normal in the infarct+captopril group. Conclusions-Chronic postinfarction endothelium-induced coronary vasodilatation is impaired, and both EE and myocap VE dysfunction contribute to myocardial depression. Captopril use prevents these abnormalities and the reduction of cardiac ecNOS mRNA.

Activation of cardiac endothelium as a compensatory component in endotoxin-induced cardiomyopathy: role of endothelin, prostaglandins, and nitric oxide.

BACKGROUND: In view of growing evidence of an important endothelial paracrine regulation of cardiac function, the present study investigated the role of cardiac endothelium-derived endothelin-1 (ET-1), prostaglandins, and nitric oxide (NO) during endotoxin-induced cardiomyopathy in rabbits. METHODS AND RESULTS: Immunohistochemical studies showed a marked transient coinduction of the inducible isoforms of NO synthase (NOS-2) and cyclooxygenase (COX-2) in endocardial endothelium and coronary arteriolar endothelium of hearts 12 hours after intravenous administration of lipopolysaccharide (LPS+12h); staining for both isoforms was much weaker 24 hours later (LPS+36h). Nitrotyrosine localization was similar to that of NOS-2, suggesting a NOS-2-related endothelial formation of peroxynitrite in septic hearts. Contractile performance of papillary muscles was depressed in both LPS-treated groups. In the LPS+12h group, however, isometric twitches were significantly prolonged (482+/-14 versus 420+/-14 ms in the saline-treated group, P<0.005). This twitch prolongation was completely reversed by simultaneous administration of BQ-123 and indomethacin to block endogenous ET-1 and prostaglandins, respectively. In addition, in the LPS+12h group, myocardial inotropic responsiveness to exogenous ET-1 was enhanced (P<0.01). CONCLUSIONS: Cardiac endothelial activation and myocardial sensitization to endothelium-derived mediators may be part of an adaptive response in the early (12 hours) stages of septic cardiomyopathy.

Cardiac endothelium and myocardial function.

Endocardial endothelium and vascular endothelium of myocardial capillaries share common features as modulators of cardiac performance, rhythmicity and growth. Growing evidence suggests differences between these two cardiac endothelial cell types with regard to developmental, morphological and functional properties. A major difference probably resides in the way and extent by which these endothelial cells perceive and transmit signals.

Exposure to oxidized low-density lipoprotein in vivo enhances intimal thickening and selectively impairs endothelium-dependent dilation in the rabbit.

OBJECTIVES: Based on in vitro studies, oxidized low-density lipoprotein (oxLDL) has been implicated in atherogenesis and the associated deficiency in endothelium-dependent relaxation. The aim of this study was to investigate the effects of in vivo exposure to oxLDL on intimal thickening and relaxing behaviour. METHODS: Intimal thickening was evoked by the placement of silicone collars around the carotid arteries of the rabbit for 3 or 14 days. OxLDL (Cu(2+)-oxidized, 7 micron/h) or the vehicle phosphate-buffered saline (PBS) was infused in the collars via subdermally implanted osmotic minipumps. RESULTS: The collared vessels receiving PBS developed discrete intimal thickening after 14 days (intima/media (I/M) ratio 11 +/- 2%). OxLDL infusion resulted in intimal thickening after 3 days and significantly enhanced the intimal thickness by 14 days (I/M ratio 98 +/- 16%). Collaring alone for 3 or 14 days and 3 days exposure to oxLDL did not impair the endothelium-dependent relaxations to acetylcholine or calcium ionophore, nor to the NO donors glyceryl trinitrate (GTN) and S-nitroso-N-acetylpenicillamine (SNAP). However, the sensitivity to acetylcholine was decreased after exposure to oxLDL for 14 days (-logEC50 oxLDL 6.95 +/- 0.11 vs. 7.52 +/- 0.11 collar alone) and the maximal relaxation to the endothelium-dependent agonist was reduced by 50%, this in the presence of a virtually intact endothelium. Complete relaxation was still obtained with the nitric oxide donors. CONCLUSION: Our results show for the first time that local vascular exposure to oxLDL in vivo promotes intimal thickening and inhibits endothelium-dependent dilation, thereby supporting an active role for oxLDL in the morphological and functional changes observed in atherosclerotic blood vessels.

The arrest of cell migration in the chicken blastoderm: experimental evidence for the involvement of a band of extracellular fibrils associated with the basal lamina.

This article overviews our current knowledge of the occurrence and distribution of oriented extracellular fibrils associated with the basal lamina, and their presumptive role in contact guidance of cells in early embryos. To investigate the role of the band of extracellular fibrils situated at the basal side of the epiblast at the cranial edge of the area pellucida of the chicken blastoderm, we determined the precise location and morphology of the fibrils using TEM and SEM, described the relationship between migrating mesoblast cells and the fibrillar band, and, finally, tested experimentally the behavior of homologous and heterologous tissues in the vicinity of the fibrillar band. The descriptive analysis demonstrated that a horseshoe-shaped, 170 microns-wide band of fibrils occurs at the cranial and lateral edges of the area pellucida and area opaca, the highest density being found in the area pellucida. Migrating mesoblast cells presented a surface morphology that was different from the morphology of cells reaching the fibrils at the lateral edge of the area pellucida. Mesoblast cells never crossed the fibrils, an observation that may explain why during gastrulation, mesoblast cells invade the area opaca only in the caudal region, where no fibrillar band is present. The experimental analysis, which involved transplantation and healing experiments, demonstrated that the arrest of cell migration, that occurred in all cases in the vicinity of the fibrillar band, was correlated with changes in surface morphology suggesting a decreased cell adhesion to the fibrils. From these observations emerged the view that the horseshoe-shaped fibrillar band functions as a barrier inhibiting migration of individual mesoblast cells and expansion of tissue sheets, rather than as an extracellular substrate mediating the oriented guidance of cells. In addition to its inhibitory role in cell migration, the extracellular band may also be regarded as a factor that stabilizes the polarity of the early embryo by determining the cranial and lateral limits between embryonic and extraembryonic tissues.

Contractile responses of isolated bovine retinal microarteries to acetylcholine.

The contractile responses of isolated and activated bovine retinal microarteries (BRA) (diameter, 204 +/- 4 microns; n = 48) to acetylcholine (ACh) were studied. These responses depended on the nature of the activating agent. The ACh relaxed BRA activated by prostaglandin F2 alpha (PGF2 alpha) and circumferential stretching in a dose-dependent manner but had no significant effect on K(+)-activated BRA. The effects of ACh also depended on the degree of BRA activation: the stronger the PGF2 alpha-induced contractions, the weaker the relaxation produced by ACh. In equivalent PGF2 alpha-induced contractions, the ACh effects were reproducible. The muscarinic antagonist, atropine, reversed the relaxation caused by ACh of PGF2 alpha-activated BRA. Physostigmine, an inhibitor of acetylcholinesterase, did not potentiate or prolong the relaxant action of ACh. Selective removal of the BRA endothelium (by gassing the BRA lumen, checked by scanning electron microscopy) blocked the relaxation caused by ACh of PGF2 alpha-induced contractions and unmasked a constricting action of ACh. This suggests that, in BRA with functional endothelium, the direct constricting effects of ACh on smooth muscle are masked by the more potent dilating activity, mediated by endothelial muscarinic receptors. Acetylcholinesterase was not found in BRA.

Effects of beta-antagonists on contraction of bovine retinal microarteries in vitro.

Contractile responses of bovine retinal microarteries (BRA) (diameter: 198 +/- 5 microns, n = 49) to beta-antagonists, local anesthetics and Ca2(+)-antagonists were studied in vitro. Propranolol (10(-8)-10(-5) M) relaxed K(+)-activated BRA dose-dependently, whereas timolol (10(-8)-10(-5) M) relaxed K(+)-activated BRA only weakly at the highest doses. The relaxation by propranolol was not mediated through interaction with adrenergic nerve endings, since fluorescence histochemistry showed absence of such nerve endings in BRA. In addition, propranolol still relaxed BRA which were treated with 6-hydroxydopamine (6-OHDA), which causes chemical adrenergic denervation. Local anesthetic properties of propranolol had no part in the relaxation: lidocaine (10(-7)-10(-5) M) did not relax K(+)-activated BRA. Verapamil (10(-9)-10(-6) M) relaxed K(+)-activated BRA markedly and dose-dependently. Both verapamil and propranolol relaxed phasic K(+)-induced force more than tonic force. By contrast, they relaxed only the tonic part of serotonin-induced force, and they had no effect on stretch-induced active force. Therefore: 1) propranolol dilates BRA more than does timolol, possibly because of the Ca2(+)-antagonistic properties of the former; 2) beta- and Ca2(+)-antagonists probably spare myogenic autoregulation of blood flow and do not prevent, but could partially reverse, serotonin-induced arterial spasm.

Distribution and turnover of testicular hyaluronidase sensitive macromolecules in the primitive streak stage chick blastoderm as revealed by autoradiography.

Primitive streak stage chick blastoderms were cultured for 30 min on a medium containing tritiated glucosamine. Light microscope autoradiography revealed extracellular labeling, and pretreatment of the sections with testicular hyaluronidase suggested the glycosaminoglycan nature of the labeled products. After incorporation of the tritiated precursor, some blastoderms were transferred to a chase medium, and cultured for 30, 90, 210 min. The changes is distribution of the labeled testicular hyaluronidase-sensitive macromolecules during the chase experiment illustrated the ingression of cells in the primitive streak stage chick blastoderm. Grain density differences, resulting from the various chase periods, suggested the renewal of the testicular hyaluronidase-sensitive fraction.

Alcian blue staining during the formation of mesoblast in the primitive streak stage chick blastoderm.

The distribution of alcian blue (AB) positivity, and its sensitivity to streptococcal and testicular hyaluronidase, were studied in primitive streak stage chick blastoderms. Accumulation of hyaluronate was observed in deep layer (DL) cells and on laterally migrating middle layer (ML) cells. During the formation of the middle layer, a first stage, namely de-epithelialization of the upper layer cells, is recognized and correlated with the absence of hyaluronate. A second stage, namely migration of the de-epithelialized upper layer cells laterally to the edge of the area pellucida, is correlated with the accumulation of AB-positivity. The AB-staining also demonstrated the accumulation of both sulphated and not-sulphated mucopolysaccharides, where a basal lamina is present.

The dorsal surface of the animal pole of the just laid quail egg, studied with SEM.

The epiblast and the surface of the perigerminal yolk of the just laid quail blastoderm were examined by scanning electron microscopy (SEM). The dorsal surface structures are microvilli, mainly along the cell borders. The scarcity of the dimples does not support that ingression occurs at this stage. Flat or round cells on the epiblast are possibly deep layer cells that failed to incorporate after passing through the epiblast. The majority of the blastoderms have an irregular margin. The large edge cells possess microvilli at their borders only. A few blastoderms, probably the more developed, have a smooth edge with closely packed cells. The margin of these germs shows round cells and lamellae that could be protruded by deep cells. The process of cell rounding and extension of lamellae may be the onset of the formation of the margin of overgrowth. Concentric zones are present on the surface of the perigerminal yolk, on which microvilli and blebs are found near the germ. The presence of cell projections on the perigerminal surface suggests its living nature.

The subgerminal yolk surface and its relationship with the inner germ wall edge of the stages X to XIV chick and quail embryo. A SEM study.

SEM reveals that the subgerminal yolk surface of the chick and quail embryo during stages X to XIV possesses microvilli and small pits. Threadlike extensions and globular structures are found on the subgerminal yolk surface mainly in the central area. The cellular nature of the subgerminal yolk was confirmed with TEM that showed the presence of a plasma membrane, mitochondria, micro-invaginations and microfilaments. The ventral cells of the germ wall are yolky and can be attached to the subgerminal yolk surface with filopodial extensions during stages X to XII. From stage XIII, the shape of these cells is usually more flattened and they protrude lamellae and filopodia.

Improved endothelial viability of heart valves cryopreserved by a new technique.

The aim of this study was to compare different techniques of aortic valve cryopreservation by studying the viability of the endothelial cells. Viability was assessed by measuring their in vitro prostacyclin (PGI2) production under basal and stimulated conditions. Fresh and cryopreserved porcine valves were incubated at 37 degrees C in tissue culture medium and PGI2 content in the medium was measured every 15 min up to 300 min. Cryopreservation by the older procedure A included 5% fetal calf serum (FCS) in the preservation medium, a plastic box inside a freezing plastic bag, a cooling schedule approximating -2 degrees C/min, a long thawing time and few dilution steps of the cryoprotectant dimethylsulphoxide (DMSO). The newer procedure B differed from A in packaging, freezing and thawing rates and DMSO dilution. Procedure C was similar to B with the exception that FCS was omitted. Leaflets preserved by procedure A produced significantly less prostacyclin as compared to those treated according to procedures B or C. We conclude that minor differences in the cryopreservation method can become critical to endothelial functional viability.

Mechanisms of endocardial endothelium modulation of myocardial performance.

The nature of modulation of myocardial performance by the endocardial endothelium (EE) is briefly described. Possible mechanisms of this modulation include a physical barrier effect, the release of various chemical messengers and a transendothelial physicochemical barrier.

The cholecystokinin CCK2 receptor antagonist, JNJ-26070109, inhibits gastric acid secretion and prevents omeprazole-induced acid rebound in the rat.

BACKGROUND AND PURPOSE: JNJ-26070109 [(R)4-bromo-N-[1-(2,4-difluoro-phenyl)-ethyl]-2-(quinoxaline-5-sulfonylamino)-benzamide] is a novel antagonist at cholecystokinin CCK(2) receptors with good pharmacokinetic properties and represents a novel mechanism for the treatment of gastro-oesophageal reflux disease (GORD). The purpose of the present study was to determine whether chronic treatment with JNJ-26070109 could prevent, as well as treat, acid rebound in rats. EXPERIMENTAL APPROACH: A chronic fistula was surgically inserted into the stomach of rats to enable the measurement of acid secretion under basal, pentagastrin and histamine-stimulated conditions. JNJ-26070109 and omeprazole were administered separately and in combination. KEY RESULTS: Sustained administration of omeprazole alone and in combination with JNJ-26070109 inhibited gastric acid secretion by >90%. However, 3 days after withdrawing treatment, there was a rebound hypersecretion by ∼1.5-fold in omeprazole-treated animals. No such acid rebound was observed with JNJ-26070109 alone or with co-administration of JNJ-26070109 and omeprazole. The anti-trophic effects of JNJ-26070109 in the gastric mucosal paralleled the effects on acid rebound. Administration of JNJ-26070109 for 3 days after cessation of omeprazole prevented the occurrence of acid rebound. Interestingly, chronic, but not acute, treatment with JNJ-26070109 also inhibited histamine-stimulated acid secretion. CONCLUSIONS AND IMPLICATIONS: Chronic administration of JNJ-26070109 effectively inhibited gastric acid secretion and suppressed proton pump inhibitor (PPI)-induced acid rebound in the rat. This work advances the field by demonstrating that modest doses of a competitive CCK(2) receptor antagonist have significant and functionally important anti-trophic actions in the gastric mucosa. These properties make JNJ-26070109 a suitable candidate for clinical investigation for the treatment of GORD.

R306465 is a novel potent inhibitor of class I histone deacetylases with broad-spectrum antitumoral activity against solid and haematological malignancies.

R306465 is a novel hydroxamate-based histone deacetylase (HDAC) inhibitor with broad-spectrum antitumour activity against solid and haematological malignancies in preclinical models. R306465 was found to be a potent inhibitor of HDAC1 and -8 (class I) in vitro. It rapidly induced histone 3 (H3) acetylation and strongly upregulated expression of p21waf1,cip1, a downstream component of HDAC1 signalling, in A2780 ovarian carcinoma cells. R306465 showed class I HDAC isotype selectivity as evidenced by poor inhibition of HDAC6 (class IIb) confirmed by the absence of downregulation of Hsp90 chaperone c-raf protein expression and tubulin acetylation. This distinguished it from other HDAC inhibitors currently in clinical development that were either more potent towards HDAC6 (e.g. vorinostat) or had a broader HDAC inhibition spectrum (e.g. panobinostat). R306465 potently inhibited cell proliferation of all main solid tumour indications, including ovarian, lung, colon, breast and prostate cancer cell lines, with IC50 values ranging from 30 to 300 nM. Haematological cell lines, including acute lymphoblastic leukaemia, acute myeloid leukaemia, chronic lymphoblastic leukaemia, chronic myeloid leukaemia, lymphoma and myeloma, were potently inhibited at a similar concentration range. R306465 induced apoptosis and inhibited angiogenesis in cell-based assays and had potent oral in vivo antitumoral activity in xenograft models. Once-daily oral administration of R306465 at well-tolerated doses inhibited the growth of A2780 ovarian, H460 lung and HCT116 colon carcinomas in immunodeficient mice. The high activity of R306465 in cell-based assays and in vivo after oral administration makes R306465 a promising novel antitumoral agent with potential applicability in a broad spectrum of human malignancies.

[A fi- tetracyclin resistance plasmid with specific restriction of phages on salmonella typhi, S. paratyphi B and S. typhi-murium (author's transl)]. / Ein fi- Tetrazyklin-Resistenz-Plasmid mit spezifischer Phagen-Restriktion bei Salmonella typhi, S. paratyphi B und S. typhi-murium.

Among 262 strains of Salmonella typhi from an epidemic outbreak of typhoid fever in Baden-Württemberg in 1974 2 strains were isolated which were tetracyclin resistant and showed no reactions with the Vi testphages T, D6 and VII whilst all other strains belonged to lysotype A, subtype Tananarive. It turned out that the Tc resistance in both strains was caused by a fi- R plasmid which could be transfered to other S. typhi strains, to E. coli K12, S. paratyphi B, S. java and S. typhi-murium as well as from Tc resistant E. coli K12 back to S. typhi. The Tc R plasmid introduced in S. typhi, lysotype A, caused specific restrictions of typing phages T, D6 and VII. Also, the transfer of the plasmids to strains of S. paratyphi B and S. typhi-murium resulted in restrictions of a number of typing phages. Both plasmids had identical patterns of restriction. In this pattern the Tc R plasmid differed from those described in the literature.

Endocardial endothelium in the rat: cell shape and organization of the cytoskeleton.

The cytoskeleton in endocardial endothelium of rat heart was examined by en face confocal scanning laser microscopy. In the ventricular cavity, endocardial endothelial cells had a polygonal shape and F-actin staining was generally restricted to the peripheral junctional actin band. Central F-actin bundles, or stress fibers, in endocardial endothelial cells were found on the tendon end of papillary muscles, especially in the right ventricle, and frequently in the outflow tract of both ventricles; elsewhere, stress fibers were scarce. Many endocardial endothelial cells were elongated in areas of endothelium with stress fibers, but no correlation was found between cell elongation and the number of stress fibers. An inverse correlation was found between the number of stress fibers and the surface area of endocardial endothelial cells. Shear stress as well as mechanical deformation of the surface of the ventricular wall during the cardiac cycle may affect cell shape and the organization of actin filaments in endocardial endothelial cells. Vimentin in endocardial endothelial cells formed a filamentous network with some distinct cytoplasmic and juxtanuclear vimentin bundles. No perinuclear ring of vimentin filaments was observed in endocardial endothelium. Microtubules in endocardial endothelial cells were, in contrast to endothelial cells of rat aorta, not aligned, less closely packed and originated from randomly distributed centriolar regions. The cytoskeleton has been suggested to play an important role in cellular functions of vascular endothelial cells. Accordingly, differences in the cytoskeletal organization between endocardial and vascular endothelial cells may relate to differences in functional properties.