Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 23-year-old woman developed thrombosis of the superior mesenteric vein and underwent an extensive enterectomy. She was diagnosed to have ATIII deficiency with extrahepatic portal vein thrombosis and esophagogastric varices. She was admitted to our department and underwent esophageal mucosal transection and splenectomy. Her activities of ATIII were 46%, but ATIII activities of her family were over 90%. ATIII activities during perioperative period were kept more than 70% following administration of ATIII drug. After splenectomy thrombocythemia which was over 300 x 10(4)/mm3 appeared with severe headache and slight pain of hands. She was discharged on 76th postoperative day with no complications and collapse of esophageal varices.
 ...
PMID:[A cases of antithrombin III (ATIII) deficiency associated with extrahepatic portal occlusion undergoing operation for esophgogastric varices]. 160 50

We examined the microvasculature of the 7,12-dimethylbenz(a)anthracene (DMBA)-induced rat mammary tumour by scanning electron microscopy of corrosion casts. An elaborate vascular envelope predominantly consisting of sinusoidal and venular vessels was formed around each tumour nodule. These vessels exhibited various abnormal features, whereas arterioles appeared normal. The abnormal vessels possessed many globular outpouches, possibly representing the site of angiogenesis. An additional capillary layer was seen in the marginal boundary between the tumour and host tissue. The lack of centrifugally extruding vessels in this layer may indicate a poor potency for vascular spread of tumour cells into the adjacent normal tissue. Loop-like or glomerular ingrowths were frequently found on the inner aspect of the vascular capsule, which eventually developed into a dense intranodular plexus. Intranodular vessels often showed focal narrowing, tapering and/or rupturing, possibly due to increased tissue pressure caused by proliferating tumour cells. Those surrounding necrotic portions were extremely dilated with occasional periodic varicosities. The features may be associated with the lessening of the tissue pressure resulting from tumour cell collapse.
 ...
PMID:The microvasculature of the 7,12-dimethylbenz(a)anthracene (DMBA)-induced rat mammary tumour. I. Vascular patterns as visualized by scanning electron microscopy of corrosion casts. 189 55

Ethanolamine oleate (EO) used widely in sclerotherapy against esophageal varices was studied for its pharmacological effect on blood coagulation and vascular damage in animals. Blood coagulation was completely inhibited by EO at a concentration of 0.31%. EO destroyed the endothelial cells of the vessel of dog and rat within one minute after injection into the vessels. An accumulation of fibrin and platelets on the surface of the damaged vessel was observed electron microscopically. Mural thrombus was formed in a few hours and the thrombus occluded the blood stream in the vein. From these animal experiment, intravasal injection of EO was considered to cause the disappearance of varices by the following two processes: collapse of varices because of occlusion of the blood stream and shrinking of the obstructed thrombus through organization.
 ...
PMID:The destructive effects of sclerosant ethanolamine oleate on mammalian vessel endothelium. 234 76

A 48-year-old woman presented to the emergency department in cardiovascular collapse after the onset of spontaneous bleeding from a noninflamed, nontraumatized varicose vein of the lower extremity. Despite successful immediate resuscitation she later succumbed to the sequelae of hemorrhagic shock. There was no evidence of coagulopathy or coagulation defect. No cardiovascular disease was found on autopsy. Although not common, spontaneous rupture of peripheral varicosities occurs often enough to be of concern. The pathologic lesions have been classified as acute and chronic, with acute lesions occurring in otherwise normal skin. Exsanguination from this source is not mentioned in standard texts, and only 27 cases have been reported in the literature.
 ...
PMID:Exsanguinating hemorrhage from peripheral varicosities. 333 22

Endoscopic ultrasonography (EUS) has been recently developed as a new diagnostic technique for portal hypertension. However, its conventional water-filled balloon technique is not suitable for the evaluation of esophageal varices, because the vessel lumen is compressed by the inflated balloon. Particularly for small varices, the vessel tends to collapse and is difficult to display. A miniature ultrasonic probe for use via the forceps channel in EUS has been developed and is expected to overcome this difficulty. Here we report the efficacy of this new probe in patients with esophago-gastric varices. Instead of using a water-filled balloon for an acoustic window, we displayed the EUS findings from the new probe in direct contact with gastrointestinal wall by removing air from the lumen under vacuum. Both conventional endoscopy and the new EUS were performed on 3 patients with esophageal varices. The transforceps-channel ultrasonic probe visualized grade 1 varices in addition to the larger varices, confirming this technique to be a useful method for assessing of esophageal varices. Moreover, this method does not require a specially designed endoscope for EUS, rather it can be employed in combination with conventional endoscopy. We conclude that this new technique is a preferred diagnostic technique, and it should become more widely accepted for routine clinical applications.
 ...
PMID:Endoscopic ultrasonography using a 15/20 MHz probe in a direct contact technique: evaluation and application in esophageal and gastric varices. 792 14

Methamphetamine (MA) produces selective degeneration of dopamine (DA) neuron terminals without cell body loss. While excitatory amino acids (EAAs) contribute to MA toxicity, terminal loss is not characteristic of excitotoxic lesions nor is excitotoxicity selective for DA fibers; rather, EAAs may modulate MA-induced DA turnover, suggesting that DA-dependent events play a key role in MA neurotoxicity. To examine this possibility, we used postnatal ventral midbrain DA neuron cultures maintained under continuous EAA blockade. As in vivo, MA caused neurite degeneration but minimal cell death. We found that MA is a vacuologenic weak base that induces swelling of endocytic compartments; MA also induces blebbing of the plasma membrane. However, these morphological changes occurred in MA-treated cultures lacking DA neurons. Therefore, while collapse of endosomal and lysosomal pH gradients and vacuolation may contribute to MA neurotoxicity, this does not explain selective DA terminal degeneration. Alternatively, MA could exert its neurotoxic effects by collapsing synaptic vesicle proton gradients and redistributing DA from synaptic vesicles to the cytoplasm. This could cause the formation of DA-derived free radicals and reactive metabolites. To test whether MA induces oxidative stress within living DA neurons, we used 2,7-dichlorofluorescin diacetate (DCF), an indicator of intracellular hydroperoxide production. MA dramatically increased the number of DCF-labeled cells in ventral midbrain cultures, which contain about 30% DA neurons, but not in nucleus accumbens cultures, which do not contain DA neurons. In the DA neuron cultures, intracellular DDF labeling was localized to axonal varicosities, blebs, and endocytic organelles. These results suggest that MA redistributes DA from the reducing environment within synaptic vesicles to extravesicular oxidizing environments, thus generating oxygen radicals and reactive metabolites within DA neurons that may trigger selective DA terminal loss.
 ...
PMID:Methamphetamine neurotoxicity involves vacuolation of endocytic organelles and dopamine-dependent intracellular oxidative stress. 815 68

Nourishment of arteries is accomplished by diffusion from the lumen of the vessel and from vasa vasorum. Most normal arteries have an extensive network of vasa in the adventitia that arise from branch points of parent arteries. When the thickness of arteries exceeds the ability of simple diffusion of nutrients from the lumen (larger muscular of atherosclerotic arteries), vasa extend into the media and intima. Vasa in the intima-media arise predominantly from adventitial vasa, but can arise from the lumen in vascular grafts and recanalized arteries after thrombosis. Vasa respond to vasoactive stimuli, and can regress after they vascularize arterial grafts and in response to regression of the atherosclerotic lesions. Therefore, vasa can increase blood flow to the artery wall by dilation of existing arteries or by formation of new vessels (neovascularization). Conversely, vasa can reduce blood flow to the artery wall by active constriction or by regression (involution) of existing vasa. The pathophysiological significance of vasa vasorum in normal and diseased arteries is related to their structure. Vasa in the intima-media are thin-walled endothelial cell tubes with thin or absent medial smooth muscle cells. Therefore, they are prone to collapse and rupture in response to arterial pressure, mechanical forces in the artery, necrotic substances found in diseased arteries, and vasospasm. Vasa also provide the artery with a vast absorptive endothelial surface that may have important implications for arterial lipid kinetics, and delivery and removal of neurohumoral agents from the artery wall. These properties have lead to speculation about their role in the pathogenesis of atherosclerosis, plaque rupture and thrombosis, medial ischemia leading to arterial dissection and aneurysm, restenosis after angioplasty, and post-stenotic dilatation. Finally, larger veins also have an extensive network of vasa that have been implicated in the pathogenesis of venous thrombosis and varicose veins.
 ...
PMID:[The vasa vasorum of the arteries]. 898 46

Portable percutaneous cardiopulmonary support (PCPS) with heparin-coated circuits and a biopump was employed in a patient who had a massive pulmonary embolism with circulatory collapse after stripping of varicosities of the leg. Emergency pulmonary embolectomy was successfully performed. The main pulmonary incision was facilitated by cross-clamping of the main pulmonary arterial root. The bypass circuit was kept closed, and used with the normothermic beating heart without converting to conventional total cardiopulmonary bypass. Blood flow from the lung was removed by pump suction, stored in the reservoir, and intermittently returned to the venous circulation. Heparin was added to the circuits to keep the activated clotting time greater than 300 sec. In massive pulmonary embolism, PCPS is useful for preoperative, intraoperative, and postoperative support.
 ...
PMID:Pulmonary embolectomy for acute massive pulmonary embolism under percutaneous cardiopulmonary support. 1022 7

Platelet-activating factor (PAF), a phospholipid signaling molecule found in brain, modulates several neural functions and is implicated in the human developmental brain disorder Miller-Dieker Lissencephaly (MDL). Exposure to PAF, and a non-hydrolyzable analogue, methyl carbamyl PAF (mc-PAF), produces the following rapid, reversible effects upon cultured hippocampal neurites: growth cone collapse, neurite retraction, and neurite varicosity formation. In this study, the cytoskeletal alterations that mediate these shape changes were investigated by comparing the effects of mc-PAF with other cytoskeletal-altering drugs, through the fluorescent labeling of cytoskeletal proteins and mitochondria, and by electron microscopy. Results indicate that rearrangements of microtubules (MTs), F-actin, and mitochondria underlie the neurite shape changes produced by mc-PAF. Evidence for MT alteration was obtained by comparing the effects of mc-PAF with nocodozole and taxol. Exposure to nocodazole, a MT-depolymerizing agent, produced growth cone collapse and neurite varicosity formation similar to mc-PAF, whereas pre-incubation of neurites in taxol, a MT-stabilizing drug, was effective in blocking mc-PAF-induced neurite effects. Immunofluorescent labeling and EM revealed MT splaying and unbundling within neurite varicosities following mc-PAF treatment. Immunofluorescent labeling also revealed that F-actin shifted from concentration in the growth cone to a diffuse distribution along the neurite shaft following mc-PAF exposure. Fluorescent labeling and EM also revealed retrograde movement and morphological alterations of mitochondria following mc-PAF exposure, resulting in mitochondrial aggregates within neurite varicosities. These cytoskeletal rearrangements may provide insights into the mechanisms by which PAF influences neuronal activity, and could have important implications for the impairment of neuronal motility observed in MDL.
 ...
PMID:Neuronal cytoskeletal alterations evoked by a platelet-activating factor (PAF) analogue. 1037 35

We had surgically treated varicose veins in 554 legs of 386 patients as of June 30, 2000. Varicose veins of the stem or segment type without skin changes were treated with sclerotherapy combined with high ligation, while a part of secondary varicose veins and the reticular or web type were treated with sclerotherapy alone. This paper describes our methods for day surgery for this condition. The most important therapeutic consideration in the surgical procedure is achieving sufficient venous collapse to prevent the occurrence of intravenous thrombus. In our 386 patients, a massive intravenous thrombus that was resected occurred in one limb (0.1%). Postoperative bleeding also occurred in one limb (0.1%) of a patient with severe liver cirrhosis.
 ...
PMID:[Day surgery for treatment of varicose veins in the leg]. 1110 1


1 2 3 Next >>