Successful embolization of a large superior gluteal artery pseudoaneurysm emerging during anticoagulant therapy

Gross hemorrhage is the most serious complication of anticoagulant therapy. We report the discovery and treatment of a large pseudoaneurysm of the superior gluteal artery in one patient who had been receiving oral anticoagulant therapy. We diagnosed the pseudoaneurysm by contrast-enhanced computed tomography, and embolized the artery with stainless steel coils. The exact cause of the pseudoaneurysm remains unclear, however, minor trauma appears most likely.     

Synaptic reorganization in the medial amygdaloid nucleus after lesion of the accessory olfactory bulb of adult rat. II. New synapse formation in the medial amygdaloid nucleus by fibers from the bed nucleus of the stria terminalis

The rearrangement of terminations from the bed nucleus of stria terminalis (BST) was examined in the medial amygdaloid nucleus (MAN) at 2 months following the lesion of the accessory olfactory bulb (AOB) using an electron microscopy and degeneration study. At 2 days following a BST lesion, the number of degenerating synapses was 0.7 ± 0.1 (mean±S.E.M.) per unit area (2500 μm² in the molecular layer, and 3/0 ± 0.3 in the cellular part. At 2 months after an AOB lesion, the degenerating synapses from the AOB had completely disappeared from the MAN. The BST was then lesioned at 2 months after the AOB lesion and, 2 days following this BST lesion, the degenerating synapses were counted in MAN. The numbers observed were 3.3 ± 0.6 per unit area in the molecular layer and 4.5 ± 0.4 in the cellular part. Therefore, the number of these degenerating synapses increased significantly within the molecular layer, though, in the cellular part the number of synapses was not significantly elevated over control. No differences in postsynaptic profiles (ratio of synapses on dendritic spine to dendritic shaft) were observed after the AOB lesion. These results indicate that the BST fibers formed new synapses in the molecular layer following the denervation of AOB fibers. The possibility of new synapse formation by other afferent fibers in addition to the AOB fibers is discussed as is the relationship between lesion induced synaptic reorganization and functional recovery after injury.     

Segmental hyperintensity on T1-weighted MRI of the liver: Indication of segmental cholestasis

The purpose of this study was to determine the relationship between segmental hyperintensity of the liver on T1-weighted images and segmental cholestasis in patients with obstructive jaundice. T1-weighted and T2-weighted MR images were obtained of 73 patients with obstructive jaundice caused by various diseases. Fat-suppressed T1-weighted images were also obtained of 10 patients. Eleven patients with segmental intra-hepatic bile duct dilatation (cholestasis) showed segmental hyperintensity on T1-weighted images and/or fat-suppressed T1-weighted images and no signal intensity difference on T2-weighted images. Sixty-two patients with widespread intrahepatic bile duct dilatation showed no intensity difference on T1-weighted and T2-weighted images (P < .01). Segmental hyperintensity on T1-weighted images was correlated with intrahepatic cholestasis.     

Functional innervation patterns in the corpus spongiosum and glans in the dog

The neural control of smooth muscle cells in the corpus spongiosum, helicine artery and bulbus glandis of the dog was investigated in relation to the mechanism involved in erection, using isometric tension recording and micro-electrode methods. In the corpus spongiosum, field stimulation evoked twitch-like contractions followed by relaxations. These relaxations were enhanced and prolonged by neostigmine and partly suppressed by atropine. Guanethidine abolished the twitch-like contractions and increased muscle tone. The relaxations observed after pre-treatment with guanethidine were abolished by tetrodotoxin (TTX), thereby indicating that these muscles are innervated by adrenergic excitatory, cholinergic and non-adrenergic non-cholinergic inhibitory nerves. In the helicine artery and bulbus glandis, field stimulation evoked contractions and these contractions were abolished by guanethidine or TTX, indicating that these muscles are innervated by adrenergic excitatory nerve fibres. After pre-treatment with guanethidine and atropine, muscle relaxation appeared in response to field stimulation in the helicine artery but not in the bulbus glandis, indicating that the helicine artery in the corpus spongiosum is also innervated by non-adrenergic non-cholinergic inhibitory nerves in addition to the excitatory adrenergic nerves. In the smooth muscle cells of the corpus spongiosum, slow potential changes were correlated with spontaneous contractions and field stimulation evoked excitatory or inhibitory junction potentials. The neural mechanism involved in erection is discussed in relation to the topical difference in the autonomic innervation patterns in the corpus spongiosum, helicine artery and bulbus glandis.     

Characterization of HPC-1 antigen, an isoform of syntaxin-1, with the isoform-specific monoclonal antibody, 14D8

We raised polyclonal and monoclonal antibodies against rat recombinant HPC-1/syntaxin 1A lacking a transmembrane domain. The polyclonal antibody recognized two major bands at 35 and 40 kDa from rat brain membranes. A hybridoma clone designated 14D8, however, recognized only one band at 35 kDa. A polyclonal antibody detected recombinant syntaxin 1B, as well as HPC-1/syntaxin 1A on an immunoblot, whereas 14D8 recognized recombinant HPC-1/syntaxin 1A, but not syntaxin 1B. Therefore, 14D8 is specific for HPC-1/syntaxin 1A. Using this monoclonal antibody, we investigated the expression of HPC-1/syntaxin 1A in the rat hippocampal membranes. HPC-1/syntaxin 1A was present even in the embryonic d 19 (E19) hippocampal membranes, and it increased during the next two postnatal wk. Pyramidal cell axons were intensely stained with the 14D8 monoclonal antibody, suggesting that HPC-1/syntaxin 1A was not restricted to the presynaptic terminal. Furthermore, we investigated the phosphorylation of HPC-1/syntaxin 1A in the rat brain membranes. HPC-1/syntaxin 1A affinity-purified on a 14D8 IgG-coupled column was recognized by antiphophoserine antibody, but not by antiphosphotyrosine and phosphothreonine antibodies.     

Lipid analysis of normal dermis and hypertrophic scars

Hypertrophic scars (HS) are a consequence of abnormal wound healing. We examined fatty acids that are contained within, and participate in, every reaction through the membrane; then, we analyzed the percentage composition of the fatty acids in deepithelialized normal dermis (ND) and HS. In vivo HS samples were obtained from six patients undergoing surgical excision, and ND samples from five patients undergoing skin grafting surgery for excess. In vitro, cultured fibroblasts from HS and ND were also analyzed. The percentage composition of fatty acids extracted from all the samples was analyzed. In vivo, arachidonic acid (20:4) was significantly more abundant in HS than in ND, in the phospholipids from both whole tissue and cell membranes. In vitro, there were no significant differences among ND, HS, and 10% fetal calf serum. The results suggest that HS formation does not necessarily involve simple excess of 20:4; however, there are considerable differences in the percentage composition of 20:4 between ND and HS. Arachidonic acid probably participates in the formation and maintenance of HS, whereas in vitro cultured fibroblasts are affected largely by fetal calf serum.     

Mild Hypercapnia Induces Vasodilation via Adenosine Triphosphate-sensitive K+ Channels in Parenchymal Microvessels of the Rat Cerebral Cortex

Background: Carbon dioxide is an important vasodilator of cerebral blood vessels. Cerebral vasodilation mediated by adenosine triphosphate (ATP)-sensitive K+ channels has not been demonstrated in precapillary microvessel levels. Therefore, the current study was designed to examine whether ATP-sensitive K+ channels play a role in vasodilation induced by mild hypercapnia in precapillary arterioles of the rat cerebral cortex.

Methods: Brain slices from rat cerebral cortex were prepared and superfused with artificial cerebrospinal fluid, including normal (Pco2 = 40 mmHg; pH = 7.4), hypercapnic (Pco2 = 50 mmHg; pH = 7.3), and hypercapnic normal pH (Pco2 = 50 mmHg; pH = 7.4) solutions. The ID of a cerebral parenchymal arteriole (5-9.5 [mu]m) was monitored using computerized videomicroscopy.

Results: During contraction to prostaglandin F2[alpha] (5 x 10-7 m), hypercapnia, but not hypercapnia under normal pH, induced marked vasodilation, which was completely abolished by the selective ATP-sensitive K+ channel antagonist glibenclamide (5 x 10-6 m). However, the selective Ca2+-dependent K+ channel antagonist iberiotoxin (10-7 m) as well as the nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester (10-4 m) did not alter vasodilation. A selective ATP-sensitive K+ channel opener, levcromakalim (3 x 10-8 to 3 x 10-7 m), induced vasodilation, whereas this vasodilation was abolished by glibenclamide.