Surgically assisted rapid maxillary expansion: a comparison of technique, response, and stability.

The purpose of this study was to evaluate the differences in treatment effects between adult patients who underwent surgically assisted rapid maxillary expansion employing buccal corticotomies and those who had midpalatal splits as well. Responses and sequelae of these treated patients were compared with adults who were expanded orthopedically and adults who were treated orthodontically without expansion. The sample comprised 37 patients who were expanded and 5 controls. Dental study casts were taken prior to treatment, at debanding, and at the posttreatment follow-up. The results indicated that maxillary expansion in adults was predictable and stable, corrected crossbites remained corrected, palatal depth was reduced in SARME, palatal width increased (more dramatically in patients treated with a combined procedure), and tipping was controlled and stable. The long-term buccogingival condition was more acceptable in adults expanded with surgical augmentation than in those expanded orthopedically.

Comparison of six commercial plasma references for factor VIII, factor IX and von Willebrand factor. On behalf of the Subcommittee for Factor VIII and IX of the Scientific and Standardization Committee of the ISTH.

Six brands of normal reference plasma produced in the United States, with assigned assay values for factor VII and IX and, in four instances, ristocetin cofactor and van Willebrand antigen, were assayed in nine coagulation laboratories in academic institutions in the same country. Differences in mean assays of reference plasmas, as a percent of labelled potency, were significant and were greater than differences among laboratories. Standard methods of assigning potency to commercial reference plasmas are recommended.

Combined multiple valve procedures and myocardial revascularisation.

We report a series of 21 consecutive patients undergoing combined multiple valve procedures and myocardial revascularisation between 1978 and 1988. There were 11 females and 10 males with a mean age of 58.5 (+/- 5.7) years. All patients were in NYHA Class 2 or more and 12 patients (57%) had angina. The mean left ventricular segment score was 7.9 (+/- 3.3). Five patients had undergone previous cardiac surgery. In all patients the aetiology of the valvular dysfunction was rheumatic. The first patient in the series was operated on using ischaemic arrest. The remaining 20 operations were performed using cardioplegia (2 crystalloid, 18 blood). A mean of 1.63 grafts per patient were inserted. There were 20 aortic valve replacements, 1 aortic valvotomy, 13 mitral valve replacements, 7 open mitral valvotomies, 1 mitral valve repair, and 1 tricuspid valve replacement. 1 patient had 3 valves replaced. Five deaths occurred in the series; all were due to low cardiac output and occurred prior to discharge from hospital. Follow-up ranged from 7 to 111 months (mean = 46 +/- 33). Three patients developed mitral paravalvular leaks, two of which were successfully repaired at 2 months and 2 years postoperatively. The third was asymptomatic. There were no late deaths and all survivors improved to NYHA Class 1 and had no angina. Early death was associated with increased perfusion time (p less than 0.01), the need for postoperative inotropic support (p less than 0.01) and high blood loss. No preoperative predictors of early death were identified. Multiple valve procedures and myocardial revascularisation carry a significant early mortality but are justified by the satisfactory long-term outcome.

The results of surgery for atrial septal defect in patients aged fifty years and over.

We examined the cases of 31 patients over the age of 50 years undergoing operative closure of isolated ostium secundum atrial septal defect. The lesion had been diagnosed in all cases prior to cardiac catheterization. To assess the importance of pre-operative data on surgical outcome, the patients were first divided into three groups according to mean pulmonary artery pressure (PAP): less than 16 mmHg (Group A), 16-30 mmHg (Group B) and greater than 30 mmHg (Group C). Symptomatic improvement occurred in all groups but more patients in Group C, although symptomatically improved, remained short of breath and in atrial fibrillation than in Group A. Patients in Group A had a higher actual forced vital capacity expressed as a percentage of the predicted value (FVCa/FVCp) than patients in Group B or Group C (P less than 0.015). There was a good correlation between FVCa/FVCp and percentage oxygen saturation of the arterial blood (P less than 0.0009). This simple non-invasive investigation was therefore found to correlate with previously documented parameters, pulmonary artery pressure and percentage oxygen saturation of the arterial blood, affecting surgical outcome. Patients were also divided into groups according to FVCa/FVCp: less than 75% (Group 1), 50-75% (Group 2) and less than 50% (Group 3). Postoperative symptoms were more common in Group 3 than in Group 1. We conclude that respiratory function tests, as well as measurement of pulmonary artery pressures, are useful in predicting improvement following atrial septal repair.

Structural and functional properties of human alpha-thrombin, phosphopyridoxylated alpha-thrombin, and gamma T-thrombin. Identification of lysyl residues in alpha-thrombin that are critical for heparin and fibrin(ogen) interactions.

alpha-Thrombin derivatives obtained either by site-specific modification at lysyl residues (phosphopyridoxylated) or by limited trypsinolysis (gamma T-thrombin) were compared to correlate structural modifications with the functional reactivity toward fibrin(ogen) and heparin. alpha-Thrombin phosphopyridoxylated in the absence of heparin (unprotected) showed approximately 2 mol of label incorporated/mol of thrombin, but only 1 mol of label incorporated/mol of proteinase when modified in the presence of added heparin (protected). In contrast to native alpha-thrombin, both phosphopyridoxylated alpha-thrombin derivatives failed to interact with a fibrin monomer-agarose column and had reduced fibrinogen clotting activity, which is very similar to gamma T-thrombin. Heparin accelerated the rate of antithrombin III inhibition of alpha-thrombin, heparin-protected modified-alpha-thrombin, and gamma T-thrombin in a manner consistent with a template mechanism but was without effect on unprotected modified alpha-thrombin. In a heparin-catalyzed antithrombin III inhibition assay of alpha-thrombin, we found that D-Phe-Pro-Arg chloromethyl ketone-active site-inactivated gamma T-thrombin competed for heparin binding. It has been shown that limited proteolysis/autolysis of the B-chain of alpha-thrombin in the area around Arg-B73 (in beta T/beta- and gamma T/gamma-thrombin), but not that around Lys-B154 (in gamma T/gamma-thrombin), diminishes specific interactions with fibrinogen (Hofsteenge, J., Braun, P. J., and Stone , S. R. (1988) Biochemistry 27, 2144-2151). In unprotected modified alpha-thrombin, lysyl residues B21, B65, B174, and B252 were phosphopyridoxylated. In heparin-protected modified alpha-thrombin, only lysyl residues B21 and B65 were phosphopyridoxylated. These observations suggest that lysyl residues 21/65 of the B-chain of alpha-thrombin are involved in fibrin(ogen) interactions, and lysyl residues 174/252 of the B-chain are important in heparin interactions.

Antithrombin activity of fucoidan. The interaction of fucoidan with heparin cofactor II, antithrombin III, and thrombin.

Fucoidan, poly(L-fucopyranose) linked primarily alpha 1----2 with either a C3- or a C4-sulfate, is an effective anticoagulant in vitro and in vivo (Springer, G. F., Wurzel, H. A., McNeal, G. M., Jr., Ansell, N. J., and Doughty, M. F. (1957) Proc. Soc. Exp. Biol. Med. 94, 404-409). We have determined the antithrombin effects of fucoidan on the glycosaminoglycan-binding plasma proteinase inhibitors antithrombin III and heparin cofactor II. Fucoidan enhances the heparin cofactor II-thrombin reaction more than 3500-fold. The apparent second-order rate constant of thrombin inhibition by heparin cofactor II increases from 4 x 10(4) (in the absence of fucoidan) to 1.5 x 10(8) M-1 min-1 as the fucoidan concentration increases from 0.1 to 10 micrograms/ml and then decreases as fucoidan is increased above 10 micrograms/ml. The fucoidan reaction with heparin cofactor II-thrombin is kinetically equivalent to a "template model." Apparent fucoidan-heparin cofactor II and fucoidan-thrombin dissociation constants are 370 and 1 nM, respectively. The enhancement of thrombin inhibition by fucoidan, like heparin and dermatan sulfate, is eliminated by selective chemical modification of lysyl residues either of heparin cofactor II or of thrombin. The fucoidan-antithrombin III reactions with thrombin and factor Xa are accelerated maximally 285- and 35-fold at fucoidan concentrations of 30 and 500 micrograms/ml, respectively. Using human plasma and 125I-labeled thrombin in an ex vivo system, the heparin cofactor II-thrombin complex is formed preferentially over the antithrombin III-thrombin complex in the presence of 10 micrograms/ml fucoidan. Our results indicate that heparin cofactor II is activated by fucoidan in vitro and in an ex vivo plasma system and suggest that the major antithrombin activity of fucoidan in vivo is mediated by heparin cofactor II and not by antithrombin III.

Calcium enhances factor Xa activity independent of gamma-carboxyglutamic acid residues.

We investigated the gamma-carboxyglutamic acid (Gla) independent effect of calcium on the activity of human factor Xa. The effect of calcium on the reaction rate of factor Xa was compared using native and Gla-modified forms of human factor Xa [chemically decarboxylated (Gla-modified, 10 Gla residues modified/mol) and Gla-domainless (chymotrypsin-treated)]. Factor Xa activity was assessed by hydrolysis of a synthetic tripeptide nitroanilide substrate, by p-aminobenzamidine binding to the active site and by inhibition with antithrombin III. Calcium (1 mM) increased, by 25-35%, the amidolytic hydrolysis rates of all three factor Xa derivatives. Calcium had an apparent Kd of approximately 200 uM with both native and modified forms of factor Xa. However, there was no change in binding of p-aminobenzamidine, a small fluorescent probe, to factor Xa in the presence of calcium. Calcium (1 mM) increased the inhibition reaction rates of native and modified forms of factor Xa with antithrombin III by 20-30%. Magnesium (1 mM) showed greatly reduced effects on factor Xa activity relative to activities with calcium. We conclude that Gla-independent calcium interactions with factor Xa are important for some catalytic activities of this blood coagulation protease.

Structure-function relationships in heparin cofactor II: spectral analysis of aromatic residues and absence of a role for sulfhydryl groups in thrombin inhibition.

This study characterizes the structural and functional significance of sulfhydryl residues in human plasma heparin cofactor II (HCII). For quantification of sulfhydryl groups, the extinction coefficient of HCII was redetermined and found to be 0.593 ml mg-1 cm-1 using second-derivative spectroscopy and multicomponent analysis assuming 4, 10, and 2 residues of tryptophan, tyrosine, and tyrosine-O-sulfate per mole of protein, respectively. The results show that tyrosine-O-sulfate residues in HCII and in cholecystokinin peptide fragments (as model compounds) do not significantly contribute to the absorbance spectrum from 280 to 300 nm. A total of three sulfhydryl groups per mole of HCII was detected by Ellman's reagent titration, with or without treatment with dithioerythritol, indicating the absence of intramolecular disulfide bonds. Incubation of HCII with 0.1-10 mM dithioerythritol did not diminish its heparin-enhanced thrombin inhibition activity. Treatment with various sulfhydryl-specific reagents, including p-mercuribenzoate, HgCl2, and N-substituted maleimide derivatives, inactivated HCII. Titration with Ellman's reagent after these reactions identified the modification site as a cysteinyl residue(s). However, complete methanethio derivatization of the sulfhydryl groups of HCII using methyl methanethiosulfonate did not alter heparin-catalyzed thrombin inhibition. These results indicate that the sulfhydryl groups of HCII are not essential for thrombin inhibition. HCII differs from antithrombin III, which contains an essential disulfide bond for heparin-dependent thrombin inhibition (Longas, M. O., et al. (1980) J. Biol. Chem. 255, 3436). Furthermore, within the "serpin" (serine proteinase inhibitor) superfamily, HCII resembles chicken ovalbumin in occurrence of sulfhydryl residues and reactivity with various sulfhydryl group-directed compounds.

Re-operation for aortic and mitral prosthetic dysfunctions.

The overall incidence of re-operation and prosthetic valve endocarditis was low in the present series as mechanical prostheses were used predominantly. The prosthetic dysfunctions were less frequent following the primary implantation with Bjork Shiley prostheses, but high operative risk was associated with the clotted Bjork Shiley prostheses. We also had unusual experience of strut fracture and sticking of Bjork Shiley discs in the closed position in both aortic and mitral positions. The early deaths were nil since the use of cardioplegic protection. Intra-operative bleeding due to adhesions can be minimised by using synthetic or heterologous pericardium during the primary operation.

Subcutaneous technique for saphenous vein harvest.

A subcutaneous technique of saphenous vein harvesting is described, and the results of its use in 37 consecutive patients requiring two or more grafts are presented. The technique minimizes the handling of the vein and reduces leg wound complications and patient discomfort.

Bone remodeling due to continuously applied loads.

It has long been known that the stress history of bone tissue influences its structure; however, the nature of this relationship remains largely uncharacterized. The objective of this work was to induce a quantifiable change in the stress history of in vivo bone tissue and examine subsequent changes in structural and material properties that might occur. Continuous compressive loads were applied to the diaphysis of adult mongrel dogs for 2 months. The loads, ranging from 12-130 N, were superposed on the normal activity of the animals by implanting spring loading devices on the diaphysis of the femur. After the animals were sacrificed, mid-diaphysial specimens were subjected to compression testing to determine a structural bulk stiffness. The cross-sectional areas of original bone tissue and new bone deposition were then determined. The ash weights of selected specimens were also determined. The results indicate that a positive correlation between the increase in cross-sectional area and the superposed stress does exist. The new bone apposition was found almost entirely on the periosteal surface. Very little evidence of internal remodeling or endosteal movement was observed. The new tissue was found to have a lower ash weight and appeared to have a disorganized microstructure. Mechanical testing also suggests that the newly deposited tissue is far less stiff than the mature original bone.