Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sarcoplasmic reticulum (SR) membrane vesicles derived from human atrium were characterized by specific ryanodine binding assay and fused into planar lipid bilayers. The tritiated form of the alkaloid bound to its receptor with a K(D) of 2.2 nM and a Bmax of 268 fmol/mg protein respectively. Special emphasis was placed on an anion-selective channel present in the SR membrane, which exhibited a mean conductance value of 67 pS when recorded in asymmetrical 50 mM trans/250 mM cis CsCl buffer system and a sensitivity to SITS (1 to 100 microM). Single and multiple channel activities displayed low voltage sensitivity and variability in its gating behavior which might result in spontaneous channel inactivation. However, the majority of the recordings (60%) resulted in a steady-state high open probability. The inactivated channel could be transiently reactivated with depolarizing voltage steps. This behavior is very similar, if not identical, to that observed for the SR Cl- channel in ventricular cells. The inactivation process is probably not directly related to a phosphorylation/dephosphorylation mechanism since PKA and PKG in presence of an adequate phosphorylation cocktail failed to reactivate the SR Cl- channel. In contrast, the use of a monoclonal anti-phospholamban antibody allowed the inhibition of the activity of the anionic channels. These results suggest that the regulation of the human atrial SR Cl- channel is dependent upon an interaction with phospholamban, which was clearly identified in our atrial preparations by Western blot analysis using monoclonal antibody.
J Mol Cell Cardiol 1996 Apr
PMID:Biochemical regulation of sarcoplasmic reticulum Cl- channel from human atrial myocytes: involvement of phospholamban. 873 4

The asymmetrical breakdown of the blood-brain barrier to Evans-blue was studied in male and female rats during epileptiform seizures and in acute hypertension. The animals were divided into six groups. Group I: control female; Group II: control male; Group III: female + acute hypertension; Group IV: male + acute hypertension; Group V: female + seizure; Group VI: male + seizure. Asymmetric breakdown of the blood-brain barrier had been seen in female rats treated with pentylenetetrazol. Pentylenetetrazol-induced seizure produces less disruption of the blood-brain barrier in right cerebral hemisphere than in left cerebral hemisphere in female rats. There were no asymmetrical changes of blood-brain barrier permeability between the left and right hemispheres in acute hypertension in both sexes, and male rats treated with pentylenetetrazol.
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PMID:Asymmetrical changes in blood-brain barrier permeability during pentylenetetrazol-induced seizures and in acute hypertension. 975 55

Early repolarization (ER) is an enigma. The purpose of this review is to reemphasize the overall electrocardiographic (ECG) pattern of this normal ST variant which continues to challenge the clinician because of its similarity to the current of injury potential to myocardium or an acute pericarditis. The data were provided from the studies identified through computerized searches of Medline, Toxline, Oxford, Agricola, and Bios Afterdark, Cumulative index, and a review of bibliographies of relevant articles on the related subjects. Early repolarization has elevated, upward, concave ST segments, located commonly in precordial leads, with reciprocal depression in a VR, tall, peaked and slightly asymmetrical T waves with notch, and slur on the R wave. The other accompanying features in the ECG are vertical axis, shorter and depressed P-R interval, abrupt transition, counterclockwise rotation, presence of U waves, and sinus bradycardia. Males dominate and patients are often younger than 50 years of age. The incidence of 1 to 2% is found equally common in all races. Degree and incidence of ST elevation decrease as age advances. Exercise or isoproterenol administration may normalize the ST segment. Early repolarization is a benign condition. If the ECG conforms to a classical pattern of ER on serial ECGs, it would exclude the unnecessary hazards of present day revascularization therapy for myocardial infarction such as primary angioplasty or thrombolytic therapy, or aggressive management of acute pericarditis, and so forth. This review concludes with a discussion of comparative ECG features of ER, pericarditis, and myocardial infarction, and provides an algorithm for diagnostic management of patients suffering from these conditions.
Clin Cardiol 1999 Feb
PMID:Early repolarization. 1006 41

A 62-year-old man was referred to our hospital for investigation of abnormal electrocardiography findings. The mean frontal plane QRS axis was directed toward the right superior quadrant(-125 degrees). Terminal S waves were present in all 3 bipolar standard leads and an R wave in lead aVR. RS complex was seen in lead V1 and deep S waves in leads V2-V6. Left ventricular hypertrophy associated with asymmetrical septal hypertrophy was suspected based on transthoracic echocardiography, but the echocardiographic quality was poor. Magnetic resonance imaging revealed hypertrophic cardiomyopathy with massive wall thickening involving the right anterobasal region of the ventricular septum. Magnetic resonance imaging may provide useful information about the distribution of ventricular myocardial hypertrophy in patients with hypertrophic cardiomyopathy and unusual electrocardiography findings.
J Cardiol 2000 Jul
PMID:Hypertrophic cardiomyopathy with dominant hypertrophy in the right anterobasal region of the ventricular septum: a case report. 1092 65

Chromanol 293B and dofetilide are inhibitors of IKs and IKr, i.e., of the slow and the rapid component of the delayed rectifier potassium current. The specificity of these drugs was tested by investigating their effects on the delayed rectifier potassium current in vascular smooth muscle, regulating the tone of blood vessels. Using depolarizing step protocols with asymmetrical potassium concentrations (135/4.5 mM K+ in pipette/bath), voltage-dependent K+ currents (IKv) of enzymatically dispersed guinea pig portal vein cells were studied in the whole-cell patch-clamp technique. Peak currents were obtained within 20 ms (at +50 mV) after activation. During a 10 s test pulse to +60 mV, these currents exhibited a relatively fast inactivation with time constants of 384 ms (Tfast) and 4505 ms (Tslow). Dofetilide was totally ineffective in modulating currents; in contrast, after application of chromanol 293B, a steady-state block of IKv developed within 135 s. The block was concentration-dependent with an IC50 of 7.4 microM. Chromanol did not produce any shift in the normalized steady-state activation and inactivation curves and the recovery from inactivation was not significantly changed. Chromanol 293B similarly inhibited delayed rectifier K+ channels whether in their closed or open state, and produced an "apparent" acceleration of inactivation, i.e., the drug accelerated the faster time constant of inactivation during a 10 s test pulse from 384 ms (control) to 149 ms (100 microM chromanol). In recent studies, chromanol was described as a specific blocker of slowly activating delayed rectifier potassium channels (IKs) in cardiomyocytes. The results of this study, however, extend the inhibitory spectrum of the drug and demonstrate block of closed and open state delayed rectifier K+ currents in portal vein vascular smooth muscle. Such a block could possibly contribute to the generation of portal hypertension.
Basic Res Cardiol 2002 Jan
PMID:Vascular effects of class-III antiarrhythmic drugs: chromanol 293B, but not dofetilide blocks the smooth muscle delayed rectifier K+ channel. 1199 73

Epidemiological associations are now well-established between insulin resistance, the metabolic syndrome and worsened cardiovascular outcomes. A direct role of insulin in vascular biology is also now broadly recognized. Specifically, insulin can directly stimulate the action of nitric oxide synthase, an effect that can be demonstrated both in vitro and in vivo. Insulin resistance, whether present endogenously or produced experimentally through exposure to fatty acids, glucosamine or tumour necrosis factor alpha, is associated with impaired endothelium-dependent vasodilation and, specifically, with impaired insulin-stimulated vasodilation. A number of potential molecular explanations for these observations are being pursued, with evidence to support a number of concurrent pathogenic mechanisms. These include insulin resistance-associated reductions in nitric oxide availability due to increases in oxidative stress (not requiring the presence of hyperglycemia), reduced availability of tetrahydrobiopterin and excess levels of asymmetrical dimethylarginine. A strong body of evidence also supports an excess of the vasoconstrictor endothelin, which may result directly from hyperinsulinemia and/or indirectly due to a loss of the suppressive effects of nitric oxide on endothelin production and action. The current leading edge of investigations into the association between insulin-resistant states and vascular dysfunction involves the expanding repertoire of adipocyte-derived hormones. Of these, particular interest has been focused on adiponectin, which has both vascular and metabolic actions, and may contribute importantly to the connection between metabolism and vascular function. Progress along these novel lines of investigation will continue to expand the understanding of the mechanisms linking insulin resistance, the metabolic syndrome and vascular disease.
Can J Cardiol 2004 Aug
PMID:Insulin resistance, metabolic syndrome and vascular diseases: update on mechanistic linkages. 1530 8

A 41-year-old man was referred to our hospital for further examination because of abnormal electrocardiography findings at a health-check examination. Transthoracic echocardiography showed left ventricular hypertrophy confined to the most distal portion of the left ventricle, which is a typical feature of apical hypertrophic cardiomyopathy. Ten years later, he was again admitted for the evaluation of chest pain. Echocardiography showed asymmetrical septal hypertrophy in addition to apical hypertrophy. These findings demonstrate morphologic evolution in hypertrophic cardiomyopathy from apical hypertrophy to asymmetrical septal hypertrophy.
J Cardiol 2005 Apr
PMID:Hypertrophic cardiomyopathy with progression from apical hypertrophy to asymmetrical septal hypertrophy: a case report. 1587 37

HOCM is a rare disorder of myocardium that may result in asymmetrical left ventricular septal hypertrophy and dynamic outflow obstruction. This may result in hemodynamic sequel that leads to deterioration of functional class in the majority of patients. Alcohol septal ablation may provide symptomatic relief in the majority of patients who fail medical therapy or who experience significantly high outflow gradients.
J Interv Cardiol 2005 Jun
PMID:Alcohol septal ablation for hypertrophic obstructive cardiomyopathy. 1596 18

We describe a 6-year-old boy with a right-sided heart part of the Kartagener syndrome, complicated by presence of a perimembranous ventricular septal defect. The defect was closed interventionally using the Amplatzer asymmetrical occluder for ventricular septal defects. The procedure was event-free. Non-operative closure of a ventricular septal defect in this patient demonstrated no other difficulty than mirror-imaged thinking, thus giving evidence that such treatment also can be offered to patients with positional anomalies.
Cardiol Young 2005 Oct
PMID:Catheter-based closure of a perimembranous ventricular septal defect using the Amplatzer occluder in a patient with right-sided heart and mirror-imaged arrangements of all organs. 1616 98

We report on a case of a 60-year-old man with progressive heart failure, mitral and aortic valve insufficiency and bilateral asymmetrical skeletal upper-limb deformities. Central to the suspicion of Holt-Oram syndrome in this patient was the surgical finding of agenesis of the left pericardium. A Holt-Oram syndrome diagnostic was confirmed through molecular analysis of the TBX5 gene. A new amino acid substitution at position 61 of the TBX5 gene was identified and confirmed the clinical diagnosis of Holt-Oram syndrome. The clinical presentation of the present case broadens the clinical spectrum of Holt-Oram syndrome and point out the importance of Tbx 5 in pericardium development. It is still an unstudied issue whether TBX5 mutations may also be present in other clinical presentations where absence of the pericardium is a feature.
Int J Cardiol 2007 Jan 02
PMID:Holt-Oram syndrome presenting as agenesis of the left pericardium. 1637 38


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