Spinal-cord stimulation in management of angina.
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Angina, Unstable↗
Biomedical subjects
A Chauhan
Publications and source records attributed to A Chauhan.
Binding of gelsolin, a secretory protein, to amyloid beta-protein.
Soluble amyloid beta-protein (Abeta) is normally present in the cerebrospinal fluid (CSF) and plasma. However, it is fibrillized and deposited as plaques in the brains of patients with Alzheimer's disease. Cerebrospinal fluid (CSF) contains several circulating proteins (apolipoprotein E, apolipoprotein J, and transthyretin) that bind to Abeta. We report here that gelsolin, a secretory protein, also binds to Abeta in a concentration-dependent manner. Under similar conditions, other proteins such as G-actin, protein kinase C, polyglutamic acid, and gelatin did not bind to Abeta. Solid phase binding assays showed two Abeta binding sites on gelsolin that have dissociation constants (Kd) of 1.38 and 2.55 microM. Abeta was found to co-immunoprecipitate along with gelsolin from the plasma, suggesting that gelsolin-Abeta complex exists under physiological conditions. The gelsolin-Abeta complex was sodium dodecyl sulfate (SDS)stable in the absence of reducing agent, but was dissociated when the SDS stop solution contained dithiothreitol (reducing agent). This study suggests that the function of secretory gelsolin in the CSF and plasma is to bind and sequester Abeta.
Amyloid beta-Peptides↗
The role of coronary angioplasty and stenting in acute myocardial infarction.
Despite the improvements in the pharmacological treatment of acute myocardial infarction, it is recognised that thrombolysis fails to reproduce reperfusion in a significant proportion of patients. Coronary interventional techniques have been shown to offer an alternative reperfusion strategy. There is increasing evidence that mechanical reperfusion may offer significant advantages over established thrombolytic therapy.
Angioplasty, Balloon, Coronary↗
Selective targeting of habenular, thalamic midline and monoaminergic brainstem neurons by neurotropic influenza A virus in mice.
Infections caused by influenza A virus have been proposed to be associated with neuropsychiatric complications, the mechanisms of which remain to be unravelled. We here report that a neurotropic strain of influenza A virus (A/WSN/33) introduced into the olfactory bulbs of C57BL/6 (B6) mice, selectively attacks habenular, paraventricular thalamic, and brainstem monoaminergic neurons. In the habenular and paraventricular thalamic areas, infection was followed by an almost total loss of neurons within 12 days. In the brain stem monoaminergic areas, viral gene products were eliminated from neurons by 12 days in B6 wildtype mice, but remained for at least 35 days in immunodefective TAP1 (Transporter associated with Antigen Presentation 1) mutant mice. In conclusion, we show that influenza A virus infection in the brain selectively targets regions which have been implicated in neuropsychiatric disturbances, and that this virus can remain for a significant period of time in specific regions of the brain in immunodefective mice.
ATP Binding Cassette Transporter, Subfamily B, Mem↗
Aggregation of amyloid beta-protein as function of age and apolipoprotein E in normal and Alzheimer's serum.
We compared the effect of serum from (a) 26 Alzheimer's disease (AD) patients and 22 age-matched non-demented controls (CO) with apolipoprotein E 4/4, 3/3 or 3/2 phenotypes, and (b) 17 normal young (aged 15-41 years) and 21 normal elderly (aged 64-83 years) people on in vitro aggregation of synthetic amyloid beta-protein (A beta) 1-40 by Thioflavin T fluorescence spectroscopy. A beta 1-40 aggregation in presence of serum from the normal elderly group was significantly higher as compared to the normal young group (correlation coefficient between age and A beta aggregation=0.73). However, no difference in A beta aggregation was observed in the presence of serum from AD patients and non-demented controls. There was a positive correlation between serum apo E concentrations and A beta aggregation, while there was no significant difference between different apo E phenotypes. The correlation coefficient in the AD 4/4 (0.65) was higher than the CO 4/4 group (0.04), while it was lower in the AD 3/3 group (-0.12) than in the CO 3/3 (0.39) group. These results suggest that the apo E4 allele alone may not be responsible for A beta fibril formation in AD; other factors may be involved in increasing risk for AD pathogenesis in those having the apo E4 allele. The severity of dementia and serum albumin levels also did not correlate with A beta aggregation. We propose that the age of an individual may be an important factor in determining the degree of A beta aggregation/fibrillization, and that mechanism of sequestration of A beta in serum may not be defective in AD.
Adolescent↗
Multiple coronary stenting in unstable angina: early and late clinical outcomes.
We examined clinical outcomes in 110 consecutive patients with unstable angina who underwent multiple coronary stenting over a 32-mo period. The main outcome measures were death, stroke, myocardial infarction, bypass surgery, and repeat angioplasty. The angiographic success rate was 100%, and the procedural success rate was 96%. There were no in-hospital deaths and five (4.5%) patients had a myocardial infarction prior to discharge. There were four (3.6%) stent thromboses with one (0.9%) patient requiring urgent bypass surgery and two (1.8%) requiring repeat angioplasty. At late follow-up (11.9+/-7.1 mo), there was (0.9%) death and three patients (2.8%) suffered myocardial infarction. Three (2.8%) patients underwent late bypass surgery and five (4.6%) had a repeat angioplasty. At follow-up, 86% of patients were event free. We conclude that multiple coronary stenting in unstable angina may be performed with a high procedural success rate and good long-term outcome.
Aged↗
Role of long-persisting human hepatitis E virus antibodies in protection.
The role of long-persisting HEV antibodies in humans was investigated. A well-characterized human volunteer anti-HEV (IgG) after 4 years of the recovery of the disease was passively immunized (200 mg kg-1 body wt) intramuscularly into three rhesus monkeys (nos 7, 8 and 9), while two monkeys (nos 5 and 6) were injected with normal immunoglobulin preparation (negative for anti-HEV IgG). At 16 h later all the animals were challenged intravenously with live HEV, as 10% stool extract prepared from the volunteer (positive for HEV by solid-phase immune electron microscopy). It was seen that transaminases (ALT/AST) were elevated in immunized monkeys on day 49 (no. 8), 60 (no. 7) and 86 (no. 9) after the virus challenge. On serological examination, all immunized (nos 7, 8 and 9) and one unimmunized (no. 6) monkeys were found positive for HEV IgM on day 10 post-challenge, while monkey no. 5 was negative. Further, all the animals from the immunized and unimmunized group seroconverted to HEV-IgG when tested on days 25 and 55 post-challenge. This has clearly shown that there is no protection. Therefore, these long-persisting HEV antibodies alone in humans, may not be protective in passive immunization.
Alanine Transaminase↗
Binding of amyloid beta-protein to intracellular brain proteins in rat and human.
Amyloid beta-protein (Abeta), in its soluble form, is known to bind several circulatory proteins such as apolipoprotein (apo) E, apo J and transthyretin. However, the binding of Abeta to intracellular proteins has not been studied. We have developed an overlay assay to study Abeta binding to intracellular brain proteins. The supernatants from both rat and human brains were found to contain several proteins that bind to Abeta 1-40 and Abeta 1-42. No major difference was observed in the Abeta binding-proteins from brain supernatants of patients with Alzheimer's disease and normal age-matched controls. Binding studies using shorter amyloid beta-peptides and competitive overlay assays showed that the binding site of Abeta to brain proteins resides between 12-28 amino acid sequence of Abeta. The presence of several intracellular Abeta-binding (AbetaB) proteins suggests that these proteins may either protect Abeta from its fibrillization or alternatively promote Abeta polymerization. Identification of these proteins and their binding affinities for Abeta are needed to assess their potential role in the pathogenesis of Alzheimer's disease.
Alzheimer Disease↗
Early and intermediate term clinical outcome after multiple coronary stenting.
OBJECTIVE: To examine the immediate and intermediate term clinical outcome of multiple coronary stenting. DESIGN: Consecutive patients were prospectively entered on a dedicated database. Follow up information was obtained from outpatient and telephone interviews with patients and family physicians. SETTING: A tertiary referral centre. PATIENTS: 140 consecutive patients underwent multiple coronary stenting between April 1994 and November 1996. Most patients had unstable coronary syndromes. MAIN OUTCOME MEASURES: Death, cerebrovascular accidents, myocardial infarction (MI), coronary artery bypass surgery (CABG), and repeat angioplasty (PTCA). RESULTS: The angiographic success rate was 100% and the clinical procedural success rate 93%. The mean (SD) follow up was 11.9 (7.2) months (range 2-32). The mean (SD) number of stents per patient was 2.4 (0.7). The mean (SD) number of lesions treated per patient was 1.4 (0.6). There were four in-hospital deaths (2.9%) and five patients (3.6%) had an MI before hospital discharge. All in-hospital deaths occurred in patients presenting with an acute MI and cardiogenic shock. Three patients (2.2%) had a late MI. One patient with stent thrombosis underwent emergency CABG. Three patients (2.2%) underwent late CABG. Eight patients (5.7%) had a repeat PTCA. Eighty three patients (61.5%) were asymptomatic at follow up and 121 (86.4%) were free from major clinical events. CONCLUSION: In an era of increased operator experience, high pressure stent deployment, and reduced anticoagulation with antiplatelet treatment alone, multiple coronary stenting may be performed with a high procedural success rate and good intermediate term outcome.
Adult↗
Factors secreted by activated microglia and monocytes reduce amyloidogenesis in vascular smooth muscle cells.
Smooth muscle cells cultured from amyloid-beta-affected arteries accumulate amyloid-beta peptide A beta. We now show that accumulation of "A beta" deposits in this model can be significantly reduced by culture in conditioned media from microglia and monocytes. Reduced A beta accumulation was associated with (i) lower secretion of A beta, (ii) increased secretion, but not cellular levels of amyloid-beta-precursor protein (A beta PP), and (iii) increased cell proliferation and metabolic activity. We suggest that improper regulation of A beta PP metabolism by monokines may facilitate vascular amyloidogenesis.
Amyloid beta-Protein Precursor↗
Antiplatelet rather than anticoagulant therapy with coronary stenting.
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Angioplasty, Balloon, Coronary↗
Left main intervention revisited: early and late outcome of PTCA and stenting.
We reviewed our experience with 28 unselected, consecutive patients undergoing left main coronary artery (LMCA) angioplasty who had been considered unsuitable for coronary artery bypass graft surgery (CABG). Fourteen patients (50%) had a protected LMCA circulation. Balloon angioplasty was performed in 11 patients (39.3%), and stents were implanted in 17 patients (60.7%). The procedure was elective in 22 patients (78.6%) and acute in the setting of myocardial infarction/cardiogenic shock in 6 (21.4%). The mean follow-up duration was 15.9 +/- 12 months. There were 5 early (before hospital discharge) and 4 late deaths (total 32.1%), 1 myocardial infarction (3.6%), 6 repeat angioplasties (21.4%), and 3 subsequent CABG (10.7%). All 5 early deaths occurred in patients with cardiogenic shock and unprotected circulation. The results of our study suggest that when patients have prohibitive surgical risks, elective LMCA angioplasty and/or stenting may be undertaken with a high procedural success rate. However, our data do not support intervention in the presence of acute myocardial infarction/cardiogenic shock.
Aged↗
Comparison of bailout versus elective stenting: time to reassess our benchmarks of outcome.
The aim of this study was to compare the clinical outcome of elective and bailout stenting in an era of improved stent deployment techniques and antithrombotic therapy. We retrospectively analysed 136 consecutive patients undergoing stent implantation over a 15 mo period. There was no significant difference in the follow-up duration, length of hospital stay, or the total incidence of major complications between the two groups. Bailout stenting, as compared to elective stenting, was not associated with an increased incidence of in-hospital (no death vs. 1.4%, 4.6% non-Q myocardial infarction vs. 0%, 7.7% vascular complications vs. 7.0%) or late complications (no death vs. 1.4%, no non-Q myocardial infarction vs. 2.8%, 3.1% repeat angioplasty vs. 5.6%, 1.5% coronary artery bypass surgery vs. 1.4%). Stents can be implanted in cases of failed angioplasty with a success rate similar to that of elective stent implantation with a low incidence of complications and equivalent clinical outcome.
Adult↗
Metal cations defibrillize the amyloid beta-protein fibrils.
Amyloid beta-protein (A beta) is the major constituent of amyloid fibrils composing beta-amyloid plaques and cerebrovascular amyloid in Alzheimer's disease (AD). We studied the effect of metal cations on preformed fibrils of synthetic A beta by Thioflavin T (ThT) fluorescence spectroscopy and electronmicroscopy (EM) in negative staining. The amount of cross beta-pleated sheet structure of A beta 1-40 fibrils was found to decrease by metal cations in a concentration-dependent manner as measured by ThT fluorescence spectroscopy. The order of defibrillization of A beta 1-40 fibrils by metal cations was: Ca2+ and Zn2+ (IC50 = 100 microM) > Mg3+ (IC50 = 300 microM) > Al3+ (IC50 = 1.1 mM). EM analysis in negative staining showed that A beta 1-40 fibrils in the absence of cations were organized in a fine network with a little or no amorphous material. The addition of Ca2+, Mg2+, and Zn2+ to preformed A beta 1-40 fibrils defibrillized the fibrils or converted them into short rods or to amorphous material. Al3+ was less effective, and reduced the fibril network by about 80% of that in the absence of any metal cation. Studies with A beta 1-42 showed that this peptide forms more dense network of fibrils as compared to A beta 1-40. Both ThT fluorescence spectroscopy and EM showed that similar to A beta 1-40, A beta 1-42 fibrils are also defibrillized in the presence of millimolar concentrations of Ca2+. These studies suggest that metal cations can defibrillize the fibrils of synthetic A beta.
Alzheimer Disease↗
Media from rhabdomyosarcoma and neuroblastoma cell cultures stimulate in vitro aggregation and fibrillization of amyloid beta-protein.
In vitro aggregation and fibrillization of synthetic amyloid beta-protein Abeta 1-40 was assessed in the conditioned media from rhabdomyosarcoma (CRL 1598, HTB 82, HTB 153, CCL 136), adenocarcinoma (CCL 218), neuroblastoma (SY5Y), and COS cells cultured in the absence and presence of 10% heat-inactivated fetal bovine serum (FBS). The aggregation and formation of cross beta-pleated sheet structures in Abeta was quantitated by Thioflavin T (ThT) fluorescence spectroscopy, while the morphology of Abeta fibrils was examined in negative staining in the electronmicroscope (EM). In cultures supplemented with 10% FBS, the conditioned media from CRL 1598, HTB 82, CCL 218, and SY5Y cell cultures stimulated Abeta aggregation in a time-dependent manner as compared to that of control (serum-containing medium that had not been exposed to cells). The order of stimulation was SY5Y > CRL 1598 > or = HTB 82 > CCL 218, and the stimulation was higher in 2 week cultures than in 1 week cultures. Similar studies using media from HTB 153, CCL 136 and COS cell cultures showed no effect on Abeta 1-40 aggregation. In serum-free cell cultures, only media from SY5Y and CRL 1598 could promote significant aggregation of Abeta 1-40. Negative staining in EM revealed Abeta fibril formation only with conditioned media from SY5Y and CRL 1598 cultured under serum free conditions; no Abeta fibrils were noticed in media from cell cultures supplemented with 10% FBS. We propose that both the SY5Y neuroblastoma cell line and the CRL 1598 rhabdomyosarcoma cell line may serve as experimental models for in vitro studies of extracellular aggregation and fibrillization of Abeta-protein in cell cultures, while rhabdomyosarcoma HTB 82 and adenocarcinoma CCL 218 may be models for study of Abeta aggregation only.
Adenocarcinoma↗
Both endothelium-dependent and endothelium-independent function is impaired in patients with angina pectoris and normal coronary angiograms.
BACKGROUND: The aim of this study was to investigate both endothelium-dependent and endothelium-independent vasodilatation in syndrome X patients. Recently selective impairment of endothelium-dependent function has been reported in a small number of syndrome X patients. However, other investigators have reported impaired endothelium-independent function. METHODS: We infused the endothelium-independent vasodilators papaverine and glyceryl trinitrate, and endothelium-dependent vasodilator acetylcholine in the left coronary artery of 35 patients with syndrome X and in 17 control subjects (atypical chest pain, negative exercise test, and normal coronary angiograms). Coronary blood flow was measured with an intracoronary Doppler catheter positioned in the proximal left anterior descending coronary artery, and the artery diameter was assessed using quantitative coronary angiography. RESULTS: The mean increase in coronary blood flow in response to a 12 mg dose of papaverine was significantly less in the syndrome X group (185 +/- 74% vs 411 +/- 59%, P < 0.001). The increase in coronary blood flow in response to acetylcholine, at doses of 1, 3, 10, and 30 micrograms.min-1, was also significantly lower in the syndrome X group (12 +/- 13 (P < 0.05), 41 +/- 33, 57 +/- 68, and 124 +/- 87% (P < 0.001)) as compared to the control group (76 +/- 49, 214 +/- 116, 355 +/- 115, and 361 +/- 74%). CONCLUSION: These findings demonstrate that both endothelium-dependent and endothelium-independent dilatation of the coronary microvasculature is impaired in syndrome X.
Acetylcholine↗
Modulation of cytokine production from an EpiOcular corneal cell culture model in response to Staphylococcus aureus superantigen.
The present study investigated the hypothesis that Staphylococcus aureus enterotoxin B (SEB) produces epithelial cell death and releases inflammatory cytokines that produce stromal infiltration during contact lens induced peripheral ulceration. Epithelial cells were incubated with different doses of SEB for various time periods. Culture supernatants were assayed for cytokines IL-1 beta, IL-6 and chemotactic agents IL-8 and LTB4 SEB induced the production of IL-1 beta and IL-8. Epithelial cells exposed for longer periods (48 h) with low concentrations of SEB produced significantly higher levels (P < 0.02) of IL-1 beta and IL-8 (P < 0.05) compared to a 24 h exposure. SEB did not induce the production of IL-6 and LTB4.
Cell Death↗
Exercise electrocardiogram and single vessel coronary artery disease.
The aim of this study was to assess the efficiency of exercise tests in identifying ischaemia in the territories supplied by the three main coronary arteries. We prospectively analysed 578 patients with single vessel coronary disease (> 50% stenosis in one vessel and completely normal other vessels). Patients with single vessel coronary artery disease were divided into three groups: patients with significant left anterior coronary artery disease (group 1, n = 234); patients with significant right coronary artery disease (group 2, n = 201); patients with significant left circumflex disease (group 3, n = 143). Our study, which is the largest prospective study of patients with angiographically documented single vessel coronary artery disease, suggests that the exercise electrocardiogram is a poor predictor of circumflex coronary artery ischaemia. In addition, the site of ST depression identified from the electrocardiogram was a poor predictor of the site of myocardial ischaemia. No single lead could distinguish between the three groups and the location of coronary stenosis could not be predicted by location of ST depression.
Coronary Disease↗