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P Langley

Publications and source records attributed to P Langley.

14 recordsLinked to original sources

Effect of lead exclusion for the manual measurement of QT dispersion.

To investigate the effect of different lead exclusion criteria for the manual measurement of QT dispersion (QTd). Simultaneous 12-lead ECGs from three groups of 25 subjects were studied; healthy normal subjects, subjects with a myocardial infarction, and subjects with arrhythmias. Leads were excluded with (1) small absolute T wave amplitudes, (2) small relative T wave amplitudes, and (3) small and/or large relative QT measurements. QTd was calculated as the QT range and assessed for its ability to differentiate between the normal and pathological groups. With exclusion of no leads or low absolute amplitude T waves (< 50 microV) significant differences were observed only between normal and myocardial infarct groups (P < 0.05). Significant differences between normal and both pathological groups were observed when excluding the lead with the smallest amplitude T wave or shortest QT (P < 0.05), or when two leads of either type were excluded (P < 0.005). There was good agreement between leads excluded by amplitude or QT (P < 0.01). Lead exclusion for QTd is important. Exclusion of the two smallest amplitude or two shortest QT leads from each subject produced the greatest differences between the normal and pathological groups.

Arrhythmias, Cardiac↗

Why a pomegranate?

Explore the source record for details and available documents.

Emblems and Insignia↗

Dispersion of QT intervals: a measure of dispersion of repolarization or simply a projection effect?

QT interval dispersion may provide little information about repolarization dispersion. Some clinical measurements demonstrate an association between high QT interval dispersion and high morbidity and mortality, but what is being measured is not clear. This study was designed to help resolve this dilemma. We compared the association between different clinical measures of QT interval dispersion and the ECG lead amplitudes derived from a heart vector model of repolarization with no repolarization dispersion whatsoever. We compared our clinical QT interval dispersion data obtained from 25 subjects without cardiac disease with similar data from published studies, and correlated these QT dispersion results with the distribution of lead amplitudes derived from the projection of the heart vector onto the body surface during repolarization. Published results were available for mean relative QT intervals and mean differences from the maximum QT interval. The leads were derived from Uijen and Dower lead vector data. Using the Uijen lead vector data, the correlation between measurements of dispersion and derived lead amplitudes ranged from 0.78 to 0.99 for limb leads, and using the Dower values ranged from 0.81 to 0.94 for the precordial leads. These results show a clear association between the measured QT interval dispersion and the variation in ECG lead amplitudes derived from a simple heart vector model of repolarization with no regional information. Therefore, measured QT dispersion is related mostly to a projection effect and is not a true measure of repolarization dispersion. Our existing interpretation of QT dispersion must be reexamined, and other measurements that provide true repolarization dispersion data investigated.

Adolescent↗

Massive ascitic fluid loss and coagulation disturbances after liver transplantation.

BACKGROUND & AIMS: A unique syndrome in which massive ascitic fluid loss developing 1-4 weeks after orthotopic liver transplantation (OLT) was associated with a hypercoagulable state and thrombotic complications is described. After OLT, severe coagulation abnormalities (international normalized ratio, 4.6) developed in a patient with ascitic losses of up to 12 L/day. The patient developed hypovolemia and severe systemic antithrombin III deficiency and venoocclusive disease in the graft. The aim of this study was to determine the prevalence of this syndrome after OLT. METHODS: Coagulation studies were performed in 25 additional patients with large ascitic fluid losses after OLT and in 7 cirrhotic patients not undergoing transplantation. RESULTS: All transplant recipients developed systemic deficiencies of multiple coagulation factors including antithrombin III. Markers of prothrombin activation were significantly elevated in both ascites and serum in all patients, and thrombotic complications subsequently developed in 5 patients. In the 7 cirrhotic patients, markers of prothrombin activation remained normal or minimally elevated and thrombotic complications were not found. CONCLUSIONS: Massive ascitic losses after OLT may lead to a hypercoagulable state from unreplaced losses of plasma coagulation factors into ascites and accumulation of thrombin in the systemic circulation. Hypovolemia and major coagulation abnormalities should be corrected with fresh frozen plasma, which may prevent the development of thrombotic complications.

Adult↗

Plasma atrial natriuretic peptide and renin-aldosterone in patients with cirrhosis and ascites: basal levels, changes during daily activity and nocturnal diuresis.

Measurements of plasma atrial natriuretic peptide concentrations at 8 AM showed raised levels in 21 patients with cirrhosis and ascites (10.5 +/- 0.8 pmol/L) compared with levels in 10 age-matched controls (4.1 +/- 0.64 pmol/L; p less than 0.0001). In eight patients and 10 controls, atrial natriuretic peptide, plasma renin activity, plasma aldosterone and urinary sodium excretion were measured every 4 hr for 24 hr. Subjects were mobile between 8 AM and 11 PM and supine from 11 PM to 8 AM. In controls, urinary sodium excretion was highest between 4 PM and 11 PM (19.34 +/- 3.74 mumol/min) and lowest between midnight and 8 AM (7.06 +/- 1.23 mumol/min; p less than 0.001). In patients, urinary sodium excretion was 0.63 +/- 0.14 mumol/min between 4 PM and midnight and 1.85 +/- 0.71 mumol/min (p less than 0.08) between midnight and 8 AM. In patients during the day, mean plasma atrial natriuretic peptide concentration did not change despite large individual variation, but large, sustained rises in plasma renin activity and plasma aldosterone were seen. Correlations were noted between atrial natriuretic peptide and urinary sodium excretion between midnight and 8 AM (r = 0.65; p less than 0.02) and 4 PM and midnight (r = 0.54; p less than 0.05) but not between 8 AM and 4 PM. Plasma renin activity dropped from 12.54 +/- 2.49 at midnight to 7.41 +/- 0.88 pmol/hr/ml at 8 AM (p less than 0.05); plasma aldosterone decreased from 1,032 +/- 101 to 798 +/- 56 pmol/L (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗

Assay, kinetics and properties of plasma adenosine diphosphatase. The relationship to acid and alkaline phosphatase and variations in disease.

A rapid radioassay was used to characterise the adenosine diphosphatase (ADPase) activities in human plasma. There was a major peak at pH 9.3, 80% of whose activity was attributable to non-specific alkaline phosphatase, with the remaining 20% probably due to a specific ADPase. There was also a small peak of ADPase activity at pH 4.0. Inhibitor and chromatographic studies showed that whilst much of this activity was attributable to non-specific acid phosphatase, there was a discrete acid ADPase. Assays of plasma ADPase activities in vascular disorders, including myocardial infarction, peripheral vascular disease and diabetes mellitus, reveal no alterations from control values. Activities of alkaline ADPase were elevated in both chronic and acute liver failure. Acid ADPase was also increased in chronic liver disease and it is suggested that alterations in ADPase activities in liver disorders may contribute to the haemostatic problems observed in these patients.

Acid Phosphatase↗

Albumin-coated Amberlite XAD-7 resin for hemoperfusion in acute liver failure. Part II: in vivo evaluation.

Albumin-coated Amberlite XAD-7 has been previously shown to be blood compatible in in vitro hemoperfusion experiments whith human blood. In this study, the preliminary results are reported on single hemoperfusions with albumin-coated XAD-7 resin in four patients with acute liver failure. The mean platelet count was 116+/-SE 16.3% of the initial arterial value and the mean white cell count was 96+/-SE 6.5% of initial at the end of four hours of hemoperfusion. Removal of bilirubin, phenols and substances in the middle molecular weight range by the resin was demonstrated. These preliminary results suggest albumin-coated Amberlite XAD-7 resin to be blood compatible and capable of removing protein-bound and middle molecular weight substances from patients with acute liver failure. Further clinical evaluation of repeated resin hemoperfusion is required to determine whether this treatment will be beneficial to patient survival.

Acrylic Resins↗

Scapular instability associated with brachial plexus irritation: a proposed causative relationship with treatment implications.

Brachial plexus irritation and other compression neuropathies can be diverse in their presentations and can cause a myriad of signs and symptoms. The purpose of this paper is to review the pertinent anatomy, kinesiology, and neurophysiology and to outline one possible cascade of events that may contribute to more diffuse upper extremity symptoms. Scapular instability and local myofascial trigger points resulting in possible secondary muscle imbalances are described. Their possible relationship to brachial plexus irritation in addition to the implications of the irritation are also discussed. The author postulates that proximal nerve irritation in the region of the thoracic outlet and shoulder may help to account for diffuse or unrelieved symptoms following conventional treatment of distal extremity problems in patients with occupational or cumulative trauma disorders. This paper outlines specific examination procedures for the therapist, which include upper limb tension testing, extensibility testing of the pectoralis minor, and gross manual muscle testing of the lower trapezius.

Brachial Plexus↗

Revising regulatory networks: from expression data to linear causal models.

Discovering the complex regulatory networks that govern mRNA expression is an important but difficult problem. Many current approaches use only expression data from microarrays to infer the likely network structure. However, this ignores much existing knowledge because for a given organism and system under study, a biologist may already have a partial model of gene regulation. We propose a method for revising and improving these initial models, which may be incomplete or partially incorrect, with expression data. We demonstrate our approach by revising a model of photosynthesis regulation proposed by a biologist for Cyanobacteria. Applied to wild type expression data, our system suggested several modifications consistent with biological knowledge. Applied to a mutant strain, our system correctly modified the disabled gene. Power experiments with synthetic data that indicate that reliable revision is feasible even with a small number of samples.

Gene Expression Profiling↗