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The present studies show the presence of a singular structure: a myoepithelial syncytium with the bases of the cells being embedded in a hypertrophied basal lamina containing collagen, in which bundles of muscular fibers also penetrate. The cells forming a vascular pseudo-endothelium are probably immobilised haemocytes.
A novel cDNA has been isolated from primary culture of human coronary arterial cells by a signal sequence trap method, and designated ESDN (endothelial and smooth muscle cell-derived neuropilin-like molecule). ESDN is a type-I transmembrane protein with the longest cleavable secretory signal sequence among eukaryotes. ESDN contains a CUB domain and a coagulation factor V/VIII homology domain, which reminds us of the structure of neuropilins. ESDN also harbors an LCCL domain, which is shared by Limulus factor C and Coch. Mouse and rat counterparts were also identified revealing >84% amino acid identity with human ESDN. The human ESDN gene was mapped between D3S1552 and D3S1271. Northern blot analysis showed that ESDN mRNA was expressed in various tissues; particularly highly expressed in cultured vascular smooth muscle cells. The ESDN expression was up-regulated in platelet-derived growth factor-BB-stimulated vascular smooth muscle cells in vitro and neointima of the balloon-injured carotid artery in vivo. Overexpression of ESDN in 293T cells suppressed their bromodeoxyuridine uptake. In addition, ESDN protein was strongly expressed in nerve bundles in rodents. Thus, ESDN is considered to play a role in regulation of vascular cell growth and may have a wide variety of functions in other tissues including the nervous system, like neuropilins.
The vascular development in the extensor muscles of rat forelegs from 12-day-old embryos up to 9-day-old animals was investigated with a light microscope using semithin plastic sections. On late day 12, blood vessels are distributed over the whole cross sectional area of the foreleg. On early day 13, a rearrangement of the blood vessels is visible. Now an avascular centre is enclosed by a vascularized tissue mantle, in which the muscle anlage starts developing. Few capillaries are visible within the muscle anlage. After differentiation of the muscle anlage into individual muscles the epimysium is passed by a netlike capillary plexus enwrapping the first avascular muscles. With the establishment of the perimysium on day 16 of embryonic development some capillaries are also visible within the individual muscles. The diameter of the capillaries is by far larger than the diameter of the myotubes. In older embryos the perimysium shows an increasing number of such large capillaries, whereas in the epimysium the capillaries are less frequent. In the perimysium a few additional capillaries with a small diameter of about 5 micron occur. On day 3 postpartum, small capillaries are also visible within the muscle fibre bundles. In the perimysium many large capillaries are still obvious. The vascular supply on day 9 postpartum, resembles that in adult muscles. The vascular supply of the muscles progresses from their periphery to more and more smaller compartments within the muscles, in close correlation to the establishment of the muscular connective tissue.
A case of dextrocardia in situs viscerum inversus, prior myocardial infarction, dilated cardiomyopathy with severe left ventricular systolic dysfunction, ventricular tachyarrhythmias and recurrent episodes of heart failure is described. Coronary artery bypass grafting for multivessel coronary artery disease had been previously performed; coronary and graft anatomy evaluation excluded the possibility of any further revascularization procedure. Electrocardiography showed left bundle branch block and echocardiography revealed significant interventricular mechanical dyssynchrony. After a complete vascular and cardiac anatomy evaluation, the patient was submitted to biventricular cardiac defibrillator implantation via a right approach and using conventional fluoroscopic equipment.
TAF10 is one of the TATA box-binding protein-associated factors (TAFs), which constitute the TFIID complex. We isolated a plant TAF10 ortholog from a Flaveria trinervia cDNA library, and named it ftTAF10. The ftTAF10 polypeptide contains a histone-fold motif, which is highly conserved among the TAF10s of other organisms. A transiently expressed green fluorescent protein (GFP) fusion protein was translocated into the nuclei of onion epidermal cells, suggesting that the ftTAF10 functions in nuclei. The transcript level was higher in stems and roots than in leaves, and in situ hybridization of F. trinervia seedlings revealed that the ftTAF10 transcript is accumulated abundantly in vascular tissues of hypocotyls, in the central cylinder of roots, and slightly in bundle sheath cells of leaves. Overexpression of ftTAF10 in Arabidopsis under the cauliflower mosaic virus 35S promoter caused two kinds of abnormal morphology, limitation of the indeterminate inflorescence and production of deformed leaves. These results indicate the possibility that ftTAF10 is a plant 'selective TAF' involved in the expression of a subset of vascular abundant genes, and that its appropriate gene expression is necessary for normal development.
The Arabidopsis PINHEAD/ZWILLE (PNH/ZLL) gene is thought to play an important role in the formation of the shoot apical meristem (SAM) and in leaf adaxial cell specification. To investigate the molecular mechanisms of rice development, we have isolated a rice homologue of PNH/ZLL, called OsPNH1. Around the SAM, OsPNH1 was strongly expressed in developing leaf primordia, specifically in the presumptive vascular domains, developing vascular tissues, a few cell-layers of the adaxial region, and future bundle sheath extension cells. In the SAM, only weak expression was observed in the central region, whereas strong expression was detected in the mid-vein region of leaf founder cells in the peripheral SAM domain. We produced transgenic rice plants containing the antisense OsPNH1 strand. The antisense OsPNH1 plants developed malformed leaves with an altered vascular arrangement and abnormal internal structure. These plants also formed an aberrant SAM with reduced KNOX gene expression. We examined the subcellular localization of the OsPNH1-GFP fusion protein and found that it was localized in the cytoplasm. On the basis of these observations, we propose that OsPNH1 functions not only in SAM maintenance as previously thought, but also in leaf formation through vascular development.
Eph receptor tyrosine kinases and their cell-surface-bound ligands, the ephrins, regulate axon guidance and bundling in the developing brain, control cell migration and adhesion, and help patterning the embryo. Here we report that two ephrinB ligands and three EphB receptors are expressed in and regulate the formation of the vascular network. Mice lacking ephrinB2 and a proportion of double mutants deficient in EphB2 and EphB3 receptor signaling die in utero before embryonic day 11.5 (E11.5) because of defects in the remodeling of the embryonic vascular system. Our phenotypic analysis suggests complex interactions and multiple functions of Eph receptors and ephrins in the embryonic vasculature. Interaction between ephrinB2 on arteries and its EphB receptors on veins suggests a role in defining boundaries between arterial and venous domains. Expression of ephrinB1 by arterial and venous endothelial cells and EphB3 by veins and some arteries indicates that endothelial cell-to-cell interactions between ephrins and Eph receptors are not restricted to the border between arteries and veins. Furthermore, expression of ephrinB2 and EphB2 in mesenchyme adjacent to vessels and vascular defects in ephB2/ephB3 double mutants indicate a requirement for ephrin-Eph signaling between endothelial cells and surrounding mesenchymal cells. Finally, ephrinB ligands induce capillary sprouting in vitro with a similar efficiency as angiopoietin-1 (Ang1) and vascular endothelial growth factor (VEGF), demonstrating a stimulatory role of ephrins in the remodeling of the developing vascular system.
Two monoclonal antibodies (AD-1 and AD-2) were prepared by fusion of mouse myeloma cells and lymph node cells of mice immunized with porcine adipocyte plasma membranes. Immunoprecipitation of iodinated adipocyte plasma membrane proteins followed by SDS-PAGE and autoradiography yielded protein antigens for each antibody. The AD-1 and AD-2 antigens were detected on mature adipocytes and a proportion of non-lipid-containing cells in stromal-vascular cultures. Adipocytes and associated capillary networks in subcutaneous adipose tissues as well as capillaries between the underlying muscle fiber bundles bound each antibody, whereas the AD-2 monoclonal antibody also reacted with vessels but not capillaries in liver tissues. In stromal-vascular cell cultures prepared from newborn pig subcutaneous tissue, the AD-1 and AD-2 antibodies exhibited reactivity towards 45 percent and 10 percent respectively, of cells 24 hours after seeding. On the other hand, only 4 percent and 1 percent of the cells in cultures prepared from 60 day fetal subcutaneous tissues expressed detectable amounts of the AD-1 and AD-2 antigens, respectively. In conclusion, cells along the adipogenic lineage possess cell surface antigens which may not be unique to adipogenic cells, but do exhibit differential expression among cell populations within adipose tissues. A temporal relationship between adipogenesis and angiogenesis was also demonstrated.
OBJECTIVE: To characterize the distribution of phosphodiesterase 5 (PDE-5), cGMP and cGMP-dependent protein kinase I (PKG1), and to evaluate the effect of pharmacological inhibition of PDE-5 in isolated preparations of pig and human urethra, as the nitric oxide (NO)/cGMP pathway generates the main inhibitory signals to reduce resistance in the bladder outlet and urethra during emptying of the bladder. MATERIALS AND METHODS: After obtaining ethics committee approval, urethral specimens were obtained from three female patients during cystectomy, and from young female pigs. The specimens were prepared for immunohistochemical investigations and for functional studies in organ baths. Effects of sildenafil, vardenafil and tadalafil (1 nm to 30 microm) were studied in l-noradrenaline (1 microm)-activated or spontaneously contracted preparations, and on relaxations induced by electrical-field stimulation (EFS). Levels of cGMP were determined by radioimmunoassay. RESULTS: After stimulation with the NO donor, DETA NONO-ate (1 mm), there was greater cGMP-immunoreactivity (IR) in urethral and vascular smooth muscles. There was a wide distribution of cGMP- and vimentin-positive interstitial cells between pig urethral smooth muscle bundles. There was also cGMP-IR within NO-synthase-IR endothelium. There was PDE-5 IR within the urethral and vascular smooth muscle cells, but also in vascular endothelial cells that expressed cGMP-IR. In pig and human sections, there was strong PKG1-IR in alpha-actin-IR urethral smooth muscle cells that also contained IR for cGMP. Sildenafil, vardenafil and tadalafil caused mean (sem) concentration-dependent relaxations of the pig urethra which, at 30 microm, were 80 (3)% (11 samples), 81 (5)% (12 samples) and 64 (4)% (10 samples) of the spontaneous tone. The relaxation of L-noradrenaline-contracted female human urethra was 100% in response to 10 microm sildenafil, and 85 (15)% and 47 (13)% for 30 microm of vardenafil and tadalafil, respectively (three samples). Vardenafil or sildenafil (30 microm) doubled cGMP levels in pig specimens. There were no effects on cGMP levels with tadalafil. EFS (1-32 Hz) caused l-NG-nitroarginine-sensitive relaxations of pig urethral muscle that were increased in amplitude and duration by PDE-5 inhibition. At 0.1 microm, sildenafil, vardenafil or tadalafil significantly prolonged the mean (sem) duration of the relaxation at 4 Hz by 55 (19)%, 45 (14)% and 51 (12)%, respectively. CONCLUSIONS: PDE-5-, cGMP- and PKG1-IR is widely distributed in human and pig urethral tissues. Nerve-induced relaxations of urethral preparations were enhanced at low concentrations of sildenafil, vardenafil and tadalafil, whereas there were direct smooth muscle-relaxant actions of the PDE-5 inhibitors at high concentrations. Inhibition of PDE-5 might be an interesting option to facilitate cGMP-mediated relaxation of the outflow region.
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Twenty-seven children with vascular deficit associated with the displaced posterolateral type of supracondylar fracture were explored surgically. Twenty-two children had median nerve signs. Associated clinical findings were bruising, tethering or puckering of the skin in the antecubital region, and a palpable subcutaneous medial spike of the proximal humeral fragment, indicating that the brachialis muscle was penetrated. Manipulation was avoided in such cases. At exploration, the neurovascular bundle was found trapped anterior to the fracture edge in 18 cases, dislocated behind the fracture edge in five cases, and separated by the spike in four cases. Fasciotomy of the antecubital region was performed, and the neurovascular bundle was released from entrapment. The vessel pulsated after release in 21 cases, vascular procedures were done in four, and the vessel ends were ligated in two completely lacerated vessels. Manipulation should be avoided in displaced posterolateral supracondylar fractures with neurovascular deficit when there is clinical evidence that the brachialis muscle belly has been buttonholed.
OBJECTIVE: To introduce the clinical entity of an intraneural ganglion cyst coexisting with a vascular adventitial cyst arising from the same joint. DESIGN: Retrospective review. PATIENTS: Two patients presented with predominantly deep peroneal neuropathy due to complex superior tibiofibular joint-related cysts. In addition to having peroneal intraneural ganglion cysts, these patients had vascular adventitial cysts: one involving a capsular arterial branch, the other a capsular vein [as well as a large, recurrent, intramuscular (extraneural) ganglion]. We then reviewed MRIs of 12 other consecutive cases of intraneural ganglia (10 peroneal and 2 tibial) arising from the superior tibiofibular joint that we treated, as well as other reported cases in the literature to determine if there were other (unrecognized) examples supporting the combination of clinical findings and radiographic patterns. RESULTS: Retrospective analysis of MRIs in the two surgically proven cases of peroneal intraneural ganglia with vascular adventitial cyst extension showed a common imaging pattern that we have termed "the wishbone sign," consisting of the connection of the ascending limb of the peroneal intraneural ganglion and the longitudinal limb of the vascular adventitial cyst in the axial plane. Our review suggests that vascular adventitial cyst extension occurs in a large proportion of cases of peroneal intraneural ganglia. A similar growth pattern was noted in a case of a tibial intraneural ganglion. CONCLUSIONS: The combination of intraneural and vascular adventitial cysts is understandable given our knowledge of normal and pathologic anatomy of para-articular cysts. The combination of intraneural ganglia and vascular adventitial cysts broadens the spectrum of clinical presentations of these cysts and suggests that cysts and their content can dissect from a joint along neurovascular bundles. These cases provide important evidence to support the articular theory for the pathogenesis of not only neural but vascular adventitial cysts as well.
A glyoxylic acid method using cryostat sections to demonstrate catecholaminergic fibres of the central nervous system was modified to show the extent of the adrenergic innervation in rat brown adipose tissue. It revealed prominent interlacing fluorescent parenchymal fibres surrounding individual adipocytes. The density of this network of fine fibres was not evident using earlier techniques. The new method also confirmed the dense networks of adrenergic fibres associated with arterial vessels. Its specificity was verified by simultaneously performing radioenzymatic determinations of tissue catecholamine levels and histochemical studies of brown adipose tissue from normal and sympathectomized rats. Chemical sympathectomy with 6-hydroxydopamine resulted in a pronounced decrease in brown adipose tissue and heart catecholamine (noradrenalin and dopamine) levels. Significantly, in brown adipose tissue of sympathectomized animals no fluorescence could be detected in terminal nerves of either the parenchyma or those of vascular smooth muscles. Nevertheless, some intense fluorescence was seen in axon bundles. The findings suggest that catecholamines of the parenchymal innervation form a larger proportion of the total catecholamine content of brown adipose tissue than was previously believed, provide stronger support for direct control of the function of multilocular adipocytes, and also confirm unpublished data reporting considerable dopamine content in brown adipose tissue.
Triple fixation for electron microscopy of the isthmic region of the human Fallopian tube distinguished adrenergic nerve terminals through their content of synaptic vesicles with a diameter of 50-60 nm. Non-vascular adrenergic nerves were found both outside and within smooth muscle bundles. Adrenergic varicosities, partly devoid of their Schwann cell ensheathing, frequently approached the smooth muscle cells within a distance of about 200 nm, and sometimes as close as 60-100 nm. These close contacts often occupied a considerable area of the naked varicosity. Electrical field stimulation of adrenergic nerves in the isthmic smooth muscle preparations in vitro induced an alpha-receptor mediated, frequency-dependent contractile response. The results show that the sympathetic nerves in the human Fallopian tube are able to exert a motor control of its smooth musculature, and may thus be involved in local functions essential for the normal fertilization process.
PURPOSE: We present 2 variants of the penile disassembly technique for epispadias repair that refine some details of the Mitchell technique. In some cases the urethral plate retracts and shortens, and there may be poor vascularization at the most distal portion. In addition, when the neurovascular bundles of the separated hemicorporeal glanular bodies are intact, it is difficult to achieve excellent correction of dorsal chordee. MATERIALS AND METHODS: Between 1995 and 1998 we performed the modified Mitchell technique in 11 boys 2 to 14 years old using 1 of 2 variants. For variant 1 the hemiglans and urethral plate remain connected by a small tissue bridge to avoid shortening the urethral plate and ensure a better blood supply. For variant 2 each corporeal body is dissected from the glans cap and neurovascular bundle to achieve complete mobility. This procedure enables ideal mobility of the corporeal bodies as well as curvature repair. When corporeal rotation was unsuccessful, we corrected persistent dorsal chordee using the Ransley corporotomy with corporostomy in 2 patients and with dermal grafting in 1. RESULTS: Mean followup was 17 months (range 6 to 30). Dorsal curvature was corrected in all cases. Cosmetic appearance was good. Complications included meatal stenosis and urethral fistula in 1 case each. CONCLUSIONS: Our variants of epispadias repair may be good alternatives to the Ransley and Mitchell complete penile disassembly techniques.
The VX2 carcinoma has been used extensively as an experimental model for different aspects of tumour behaviour and is usually maintained by serial intramuscular injections of tumour cells. The tumour grows rapidly, infiltrating between muscle bundles into the fibrous tissue replacing ischaemic muscle and into the vascular tree. The most interesting method of spread occurs within the sarcolemma and this may be responsible for the rounded cell nests described in this tumour.
We report a rare case of expansively growing angioleiomyoma in the proximal tibia of a 64-year-old woman. MRI revealed a well-defined area of low signal intensity on T1-weighted image and high intensity on T2-weighted image. Angiographs showed hypervascularity and vascular poolings. Microscopic examination after incisional biopsy showed an angioleiomyoma with bundles of nerve fibers.
Diaphragm disease of the small intestine is part of the spectrum of diseases associated with injury to the gastrointestinal tract induced by nonsteroidal anti-inflammatory drugs. Standard endoscopy or contrast studies of the small intestine rarely identify these lesions. The diagnosis usually is established at the time of surgery. We report the case of a 72-year-old woman with obscure gastrointestinal bleeding and intermittent obstruction of the small intestine who had had multiple hospitalizations and extensive testing. The patient had been treated with nonsteroidal anti-inflammatory drugs for osteoarthritis. A radiograph of the small intestine with barium contrast revealed no abnormalities, so capsule endoscopy was performed. Capsule endoscopy showed multiple small intestinal strictures beyond which the capsule could not pass. After the patient experienced continued symptoms suggestive of intermittent partial obstruction of the small intestine, computed tomography showed the capsule within a dilated loop of intestine adjacent to a stricture. After 9 days of conservative medical therapy and worsening symptoms, the patient required an exploratory laparotomy. The capsule was located in a 12-cm segment of intestine with 4 diaphragm-like lesions. Pathologic study found submucosal lesions with features identical to those of neuromuscular and vascular hamartoma (eg, mature, reactive tissue elements of smooth muscle, dense fibrous tissue, and nerve tissue bundles with scattered ganglion cells and vessels). No manifestations of Crohn disease were evident. This case represents the first diagnosis with capsule endoscopy of diaphragm disease of the small intestine with pathologic features of neuromuscular and vascular hamartoma.