Observation of Wakefields and Resonances in Coherent Synchrotron Radiation.

We report on high resolution measurements of resonances in the spectrum of coherent synchrotron radiation (CSR) at the Canadian Light Source (CLS). The resonances permeate the spectrum at wave number intervals of 0.074 cm(-1), and are highly stable under changes in the machine setup (energy, bucket filling pattern, CSR in bursting or continuous mode). Analogous resonances were predicted long ago in an idealized theory as eigenmodes of a smooth toroidal vacuum chamber driven by a bunched beam moving on a circular orbit. A corollary of peaks in the spectrum is the presence of pulses in the wakefield of the bunch at well-defined spatial intervals. Through experiments and further calculations we elucidate the resonance and wakefield mechanisms in the CLS vacuum chamber, which has a fluted form much different from a smooth torus. The wakefield is observed directly in the 30-110 GHz range by rf diodes, and indirectly by an interferometer in the THz range. The wake pulse sequence found by diodes is less regular than in the toroidal model, and depends on the point of observation, but is accounted for in a simulation of fields in the fluted chamber. Attention is paid to polarization of the observed fields, and possible coherence of fields produced in adjacent bending magnets. Low frequency wakefield production appears to be mainly local in a single bend, but multibend effects cannot be excluded entirely, and could play a role in high frequency resonances. New simulation techniques have been developed, which should be invaluable in further work.

Laboratory diagnosis of inherited protein S deficiency.

The authors investigated assays for free protein S (ProS) antigen, total ProS antigen, and ProS crossed immunoelectrophoresis (CIEP) in the diagnosis of type 1 inherited ProS deficiency. Accurate measurement of the hemostatically important free ProS required showing that, on each specimen, precipitation of the C4b-binding protein (C4b-BP)/protein S complex (C4b-BP/ProS) by polyethylene glycol-8,000 (PEG) was complete. The authors showed this by doing a ProS CIEP on the same PEG supernate that was used for quantitative measurement of free ProS. The +/- 2 standard deviation (+/- 2 SD) ranges for free ProS were 81-133% for males and 50-130% for females. This striking male-female difference has been reported only twice before. With the use of a graph of values for free ProS versus prothrombin time (PT), patients with inherited ProS deficiency segregated cleanly from normals and from patients on warfarin therapy without ProS deficiency until the PT was greater than 20 seconds. There is overlap of total ProS antigen values between normals and patients with inherited ProS deficiency.

Heparin cofactor II assay. Elimination of heparin and antithrombin-III effects.

Functional assays for heparin cofactor II (HC-II) are based on the inactivation of thrombin by HC-II in the presence of dermatan sulfate (DS). Residual thrombin is measured in a chromogenic assay. Interference by the antithrombin-III (AT-III)/heparin complex, which also rapidly inactivates thrombin, must be eliminated from the HC-II test system. Commercial DS is contaminated with heparin, while plasma specimens to be tested contain AT-III. After NaNO2/acetic acid treatment of DS (to inactivate heparin), there was enough residual heparin to cause AT-III interference. Treatment of plasma with commercially available anti-AT-III antiserum largely, but not completely, removed AT-III interference from the HC-II assay. With commercially available reagents, both NaNO2/acetic acid treatment of DS and anti-AT-III treatment of plasma were needed to eliminate heparin/AT-III interference. Protamine sulfate inactivated DS as well as heparin and could not be used to reduce AT-III/heparin interference with the HC-II assay.

Kallikrein inhibition and C1-esterase inhibitor levels in patients with the lupus inhibitor.

It has been suggested that kallikrein inhibition may predispose patients with the lupus inhibitor to thrombosis by interfering with the Factor XII-mediated activation of plasminogen. To further investigate this suggestion, the authors measured kallikrein inhibition in 19 patients with the lupus inhibitor. They found that kallikrein inhibition was greater than 100% of that of a normal plasma pool in all patients and greater than 125% in 11 of 19. Kallikrein inhibition was significantly correlated with C1-esterase inhibitor (C1S-INH) concentration, which they measured by rocket immunoelectrophoresis (r = +0.55, P less than 0.05). In three patients the C1S-INH was more than 30% greater than the kallikrein inhibition. Crossed immunoelectrophoresis for C1S-INH in these patients' plasma revealed an electrophoretic mobility identical with that of the normal plasma pool. The authors suggest that C1S-INH-mediated kallikrein inhibition, in conjunction with other coagulation abnormalities, predisposes patients with the lupus inhibitor to thrombosis.

Abnormal prothrombin crossed-immunoelectrophoresis in patients with lupus inhibitors.

Prothrombin deficiency has been known to occur in association with lupus inhibitors for over 25 years. We studied 21 patients with lupus inhibitors and found that four of five with prothrombin deficiency and ten of 16 with quantitatively normal prothrombin had abnormal prothrombin crossed-immunoelectrophoresis (CIEP) characterized by material moving slower in the first dimension of electrophoresis than normal prothrombin. In two patients with prothrombin deficiency, all prothrombin measured by quantitative assay and all slow-moving material on CIEP were removed by treatment with Staphylococcal protein A (SPA). These patients had free antibody, which bound to normal plasma prothrombin, forming larger amounts of slow-moving material on CIEP. A third patient with prothrombin deficiency had only partial removal of prothrombin after SPA treatment. Two patients with quantitatively normal prothrombin had all slow-moving material on CIEP and about one fourth of the prothrombin by quantitative assay removed by SPA treatment. There was no correlation among the strength of the inhibitor, the presence of a "cofactor effect," and the prothrombin abnormality. These data suggest that heterogeneous antiprothrombin antibodies, with or without prothrombin deficiency, are present in the majority of patients with lupus inhibitors.