Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a fetus of 28 weeks' gestation in which ultrasonography demonstrated unilateral ventriculomegaly and microcephaly. Fetal MRI demonstrated a simple, left paramedian occipital cyst with rarefaction of the corpus callosum and thinning of the adjacent cortical mantle. Ischaemia was suggested as the underlying pathogenesis, but autopsy after termination of pregnancy revealed a glioependymal cyst. This case highlights consideration of the rare diagnosis of glioependymal cyst when a cystic lesion associated with cerebral malformations, particularly dysgenesis of the corpus callosum, is demonstrated and fetal MRI suggests an ischaemic origin.
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PMID:Fetal MRI demonstrates glioependymal cyst in a case of sonographic unilateral ventriculomegaly. 1728 53

We sought to determine whether administration of a very low, nonvasodilating dose of a highly selective adenosine A(2A) receptor agonist (ATL-193 or ATL-146e) would be cardioprotective in a canine model of myocardial stunning produced by multiple episodes of transient ischemia. Twenty-four anesthetized open-chest dogs underwent either 4 (n=12) or 10 cycles (n=12) of 5-min left anterior descending coronary artery (LAD) occlusions interspersed by 5 or 10 min of reperfusion. Left ventricular thickening was measured from baseline through 180 min after the last occlusion-reperfusion cycle. Regional flow was measured with microspheres. In 12 of 24 dogs, A(2A) receptor agonist was infused intravenously beginning 2 min prior to the first occlusion and continuing throughout reperfusion at a dose below that which produces vasodilatation (0.01 microg x kg(-1) x min(-1)). Myocardial flow was similar between control and A(2A) receptor agonist-treated animals, confirming the absence of A(2) receptor agonist-induced vasodilatation. During occlusion, there was severe dyskinesis with marked LAD zone thinning in all animals. After 180 min of reperfusion following the last cycle, significantly greater recovery of LAD zone thickening was observed in A(2A) receptor agonist-treated vs. control animals in both the 4-cycle (91 +/- 7 vs. 56 +/- 12%, respectively; P<0.05) and the 10-cycle (65 +/- 9 vs. 8 +/- 16%, respectively; P<0.05) occlusion groups. The striking amount of functional recovery observed with administration of low, nonvasodilating doses of adenosine A(2A) agonist ATL-193 or ATL-146e supports their further evaluation for the attenuation of postischemic stunning in the clinical setting.
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PMID:Cardioprotection by adenosine A2A agonists in a canine model of myocardial stunning produced by multiple episodes of transient ischemia. 1730 4

After having reviewed the various theories explaining the mechanism of menstruation, a hypothesis is propounded by the authors, according to which during the premenstrual period, thinning of the endometrium provokes a settling of the spiral arteries, highly developed at that moment. The vascular endothelial alterations induced by this settling would be sufficient to provoke erythrodiapedesis and superficial infarction that decapitate the superficial portion of the arteriolae. Liberation of prostaglandins following this small haemorrhage would lead to vasoconstriction of basal arteries and ischemia. The subsequent reflex vasodilatation causes the ischemic endometrium to fall off.
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PMID:[A new hypothesis on the intimate mechanism of menstruation]. 1747 3

We investigated the role of kinin receptors in cardiac remodeling after ischemia/reperfusion (I/R). Bradykinin injection improved cardiac contractility, diastolic function, reduced infarct size and prevented left ventricular thinning after I/R, whereas des-Arg(9)-BK injection had no protective effects. Bradykinin, but not des-Arg(9)-BK, reduced cardiomyocyte apoptosis and increased Akt and GSK-3beta phosphorylation. Furthermore, myocardial infarct size was similar between wild type and B2 knockout mice after I/R, but significantly reduced in kinin B1 receptor knockout mice. These results indicate that the kinin B2 receptor, but not the B1 receptor, protects against I/R-induced cardiac dysfunction by inhibiting apoptosis and limiting ventricular remodeling.
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PMID:Differential role of kinin B1 and B2 receptors in ischemia-induced apoptosis and ventricular remodeling. 1764 19

Previous studies have shown that 1 wk after permanent coronary artery ligation in rats, some cellular mechanisms involving TNF-alpha occur and contribute to the development of cardiac dysfunction and subsequent heart failure. The aim of the present study was to determine whether similar phenomena also occur after ischemia-reperfusion and whether cytokines other than TNF-alpha can also be involved. Anesthetized male Wistar rats were subjected to 1 h coronary occlusion followed by reperfusion. Cardiac geometry and function were assessed by echocardiography at days 5, 7, 8, and 10 postligation. Before death, heart function was assessed in vivo under basal conditions, as well as after volume overload. Finally, hearts were frozen for histoenzymologic assessment of infarct size and remodeling. The profile of cardiac cytokines was determined by ELISA and ChemiArray on heart tissue extracts. As expected, ischemia-reperfusion induced a progressive remodeling of the heart, characterized by left ventricular free-wall thinning and cavity dilation. Heart function was also decreased in ischemic rats during the first week after surgery. Interestingly, a transient and marked increase in TNF-alpha, IL-1beta, IL-6, cytokine-induced neutrophil chemoattractant (CINC) 2, CINC3, and macrophage inflammatory protein-3alpha was also observed in the myocardium of myocardial ischemia (MI) animals at day 8, whereas the expression of anti-inflammatory interleukins IL-4 and IL-10 remained unchanged. These results suggest that overexpression of proinflammatory cytokines occurring during the first week after ischemia-reperfusion may play a role in the adaptative process in the myocardium and contribute to early dysfunction and remodeling.
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PMID:Delayed expression of cytokines after reperfused myocardial infarction: possible trigger for cardiac dysfunction and ventricular remodeling. 1787 14

The aim of the study was to evaluate the cardioprotective and antiarrhythmic effects of intravenous Na+/H+ blockers (cariporide and SM-20550) in a rat model of ischemia and a long period reperfusion (14 days). This model allowed study of the role of Na+/H+ exchanger against late myocardial infarct expansion and left ventricular dysfunction. Each compound was administered 5 min before ischemia. Cariporide (from 0.16 mg/kg) and SM-20550 (from 0.04 mg/kg) significantly and dose-dependently reduced the number of ventricular premature beats during ischemia. The duration of ventricular tachycardia was importantly shortened in the presence of cariporide (0.63 mg/kg) and SM-20550 (0.16 mg/kg). Furthermore, cariporide (0.63 mg/kg) and SM-20550 (from 0.04 mg/kg) significantly reduced the infarct expansion: 43 +/- 2% in the cariporide group and 42 +/- 2% at 0.16 mg/kg SM-20550 versus 48 +/- 1% in the vehicle group. Cariporide and SM-20550 significantly prevented the left ventricular free wall thinning associated with the thickness ratio, suggesting a significant reduction of the ventricular dilation. Cariporide and SM-20550 significantly improved the negative dP/dtmax, suggesting a partial restoration of the cardiac relaxation. Collectively, Na+/H+ blockers administered before ischemia reduced arrhythmias and also prevented the remodeling process of the heart during postinfarction.
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PMID:Effects of SM-20550 against myocardial infarction-induced arrhythmias, late infarct expansion, and left ventricular dysfunction. 1803 67

We assessed the role of nitric oxide (NO) and the kinin B2 receptor in mediating tissue kallikrein's actions in intramyocardial inflammation and cardiac remodeling after ischemia/reperfusion (I/R) injury. Adenovirus carrying the human tissue kallikrein gene was delivered locally into rat hearts 4 days prior to 30-minute ischemia followed by 24-hour or 7-day reperfusion with or without administration of icatibant, a kinin B2 receptor antagonist, or N(omega)-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor. Kallikrein gene delivery improved cardiac contractility and diastolic function, reduced infarct size at 1 day after I/R without affecting mean arterial pressure. Kallikrein treatment reduced macrophage/monocyte and neutrophil accumulation in the infarcted myocardium in association with reduced intercellular adhesion molecule-1 levels. Kallikrein increased cardiac endothelial nitric oxide synthase phosphorylation and NO levels and decreased superoxide formation, TGF-beta1 levels and Smad2 phosphorylation. Furthermore, kallikrein reduced I/R-induced JNK, p38MAPK, IkappaB-alpha phosphorylation and nuclear NF-kappaB activation. In addition, kallikrein improved cardiac performance, reduced infarct size and prevented ventricular wall thinning at 7 days after I/R. The effects of kallikrein on cardiac function, inflammation and signaling mediators were all blocked by icatibant and L-NAME. These results indicate that tissue kallikrein through kinin B2 receptor and NO formation improves cardiac function, prevents inflammation and limits left ventricular remodeling after myocardial I/R by suppression of oxidative stress, TGF-beta1/Smad2 and JNK/p38MAPK signaling pathways and NF-kappaB activation.
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PMID:Nitric oxide mediates cardiac protection of tissue kallikrein by reducing inflammation and ventricular remodeling after myocardial ischemia/reperfusion. 1806 96

Optical coherence tomography (OCT) is a rapidly emerging imaging modality that can provide non-invasive, cross-sectional, high-resolution images of tissue morphology in situ and in real-time. In the present series of studies, we used a high-speed OCT imaging system equipped with a frequency-swept laser light source (1.3 mum wavelength) to study living kidneys in situ. Adult, male Munich-Wistar rats were anesthetized, a laparotomy was performed and the living kidneys were exposed for in situ observation. We observed the kidneys prior to, during and following exposure to renal ischemia induced by clamping the renal artery. The effects of intravenous mannitol infusion (1.0 ml of 25%) prior to and during renal ischemia were also studied. Finally, living kidneys were flushed with a renal preservation solution, excised and observed while being stored at 0-4 degrees C. Three-dimensional OCT data sets enabled visualization of the morphology of the uriniferous tubules and the renal corpuscles. When renal ischemia was induced, OCT revealed dramatic shrinkage of tubular lumens due to swelling of the lining epithelium. Three-dimensional visualization and volumetric rendering software provided an accurate evaluation of volumetric changes in tubular lumens in response to renal ischemia. Observations of kidneys flushed with a renal preservation solution and stored at 0-4 degrees C also revealed progressive and significant loss of tubular integrity over time. Intravenous infusion of mannitol solution resulted in thinning of the tubular walls and an increase in the tubular lumen diameters. Mannitol infusion also prevented the cell swelling that otherwise resulted in shrinkage of proximal tubule lumens during ischemia. We conclude that OCT represents an exciting new approach to visualize, in real-time, pathological changes in the living kidney in a non-invasive fashion. Possible clinical applications are discussed.
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PMID:High-resolution optical coherence tomography imaging of the living kidney. 1826 76

Hyperbaric oxygen therapy is a primary or adjuvant therapeutic method used in treatment of various acute or chronic disorders. Currently, eye diseases are among the off-label use of hyperbaric oxygen. However, there is an increasing body of evidence showing its safety and efficacy in retinal artery occlusion, cystoid macular edema secondary to retinal vein occlusion, scleral thinning and necrosis faced after pterygium surgery, orbital rhino-cerebral mucormycosis, nonhealing corneal edema, and anterior segment ischemia. Its potential to treat some blinding disease has also been pointed out in recent studies. This article constitutes an up-to-date summary of knowledge and therapeutic use of hyperbaric oxygen, and aims to contribute understanding of current and potential use of hyperbaric oxygen therapy in ophthalmology.
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PMID:The use of hyperbaric oxygen therapy in ophthalmology. 1834 77

To describe use of a locally processed bovine pericardium (BP) to cover a large central corneal perforation following alkali injury and discuss postoperative outcome. A 27-year-old Malay male patient presented two weeks after alkali splashed in his left eye while working. A clinical diagnosis of left central corneal ulcer with limbal ischemia following alkali injury with secondary infection was made. After failed medical therapy, we performed a Gunderson conjunctival flap under local anesthesia that retracted after one week and resulted in a large central corneal perforation with surrounding stromal thinning. The perforation was covered with a locally processed BP xenograft (Lyolemb) supplied by the National Tissue Bank, University Sains Malaysia. Nine months follow-up showed a well-taken graft without any exposure/dehiscence and minimal inflammation. Amniotic membrane transplantation when used as a patch graft needs an urgent tectonic graft to promote corneal stability in patients with severe corneal thinning. The use of processed BP can be a viable option in treating such cases.
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PMID:Bovine pericardium in treating large corneal perforation secondary to alkali injury: a case report. 1871 Dec 78


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