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Biomedical subjects

S A Smith

Publications and source records attributed to S A Smith.

At least 73 records · Page 4Linked to original sources
PubMed2000

Antagonists of alcohol inhibition of cell adhesion.

Increasing evidence suggests that alcohols act within specific binding pockets of selective neural proteins; however, antagonists at these sites have not been identified. 1-Alcohols from methanol through 1-butanol inhibit with increasing potency the cell-cell adhesion mediated by the immunoglobulin cell adhesion molecule L1. An abrupt cutoff exists after 1-butanol, with 1-pentanol and higher 1-alcohols showing no effect. Here, we demonstrate surprisingly strict structural requirements for alcohol inhibition of cell-cell adhesion in L1-transfected NIH 3T3 fibroblasts and in NG108-15 neuroblastoma x glioma hybrid cells treated with BMP-7, an inducer of L1 and neural cell adhesion molecule. The target site discriminates the tertiary structure of straight-chain and branched-chain alcohols and appears to comprise both a hydrophobic binding site and an adjacent hydrophilic allosteric site. Modifications to the 2- and 3-carbon positions of 1-butanol increased potency, whereas modifications that restrict movement about the 4-carbon abolished activity. The effects of ethanol and 1-butanol on cell-cell adhesion were antagonized by 1-pentanol (IC(50) = 715 microM) and 1-octanol (IC(50) = 3.6 microM). Antagonism by 1-octanol was complete, reversible, and noncompetitive. 1-Octanol also antagonized ethanol inhibition of BMP-7 morphogenesis in NG108-15 cells. 1-Octanol and related compounds may prove useful in dissecting the role of altered cell adhesion in ethanol-induced injury of the nervous system.

3T3 Cells↗
PubMed2000

2-(Alkylthio)pyrimidin-4-ones as novel, reversible inhibitors of lipoprotein-associated phospholipase A2.

Starting from two weakly active hits from high throughput screening, a novel series of 2-(alkylthio)-pyrimidin-4-ones with high potency and selectivity for lipoprotein-associated phospholipase A2 has been designed. In contrast to previously known inhibitors, these have been shown to act by a non-covalent and substrate competitive mechanism.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed2000

In vitro studies on optimal requirements for the growth of Spironucleus vortens, an intestinal parasite of the freshwater angelfish.

Spironucleus vortens were cultivated in either an artificial medium at different temperatures, or in medium at various pH conditions or supplemented with different bile concentrations at 25 degrees C. Temperature, pH and bile requirements for the optimal growth of the parasite were determined. Parasites multiplied quickly at 28 and 31 degrees C and reached maximum numbers on Day 4 of cultivation, whereafter they did not survive. At 25 degrees C, parasites survived longer than those at 28 and 31 degrees C with no difference in multiplication rate during the exponential phase. The longest survival period was seen at 22 degrees C, although the growth rate of the parasite was not as high as those at 25 degrees C. At a higher temperature of 37 degrees C, no parasites were observed alive after the second day of cultivation. Optimal pH range for the parasite's growth was 6.5 to 7.5, with the highest cell number at pH 7.5. Parasites survived longest (15 d) at pH 6.0, although the maximum number of cells was lower than those at the optimal pH. Parasites were dead within 24 h at pH levels above 8.5 or below 5.5. All cultures supplemented with either bovine or fish bile yielded numbers of parasites lower than cultures with no bile. In addition, parasite growth was significantly suppressed in medium supplemented with higher concentrations of bile. These results indicate that the optimal condition for the in vitro cultivation of S. vortens is 25 degrees C and pH 6.5 to 7.5 without supplementation with bile.

Animals↗
PubMed2000

Effects of imidazoline binding site ligands on the growth and viability of clonal pancreatic beta-cells.

Pancreatic beta-cells express imidazoline binding sites which play a role in the regulation of insulin secretion, but it is not known whether ligands for these sites also affect other aspects of beta-cell physiology. In the present study, we have investigated the effects of a range of imidazoline reagents on the growth and viability of clonal pancreatic beta-cells (RINm5F and HIT-T15). Three imidazoline compounds (idazoxan, phentolamine and antazoline) were found to cause marked inhibition of beta-cell growth in a time and concentration dependent manner. Idazoxan was the most potent of these with as little as 0.5 microM causing a significant decrease in beta-cell viability (EC50 approximately 10 microM). All three imidazolines also decreased the viability of clonal beta-cells in parallel with their inhibitory effects on cell growth. These effects were not reproduced by any of a wide-range of other imidazoline compounds, including effective insulin secretagogues such as efaroxan and RX821002. The effects of the three ligands did not correlate with their relative potencies for binding to any of the well-characterised imidazoline binding sites nor to alpha2-adrenoceptors. In addition, the inhibitory responses were not antagonised by other imidazoline binding site ligands. The inhibitory effects of idazoxan on the growth of RINm5F and HIT-T15 beta-cells required as little as 3-h exposure to the imidazoline and were not readily reversible when the reagent was removed. Reductions in growth rate were accompanied by marked alterations in the morphology of the cells, which could be detected before loss of viability. Cells exposed to phentolamine showed the characteristic features of apoptosis in that the nuclei were condensed (as judged by acridine orange staining) and electrophoresis of DNA revealed the presence of oligonucleosomal fragmentation. These changes could not be detected in cells exposed to idazoxan despite the more profound reduction in viability induced by this agent. We conclude that a sub-group of imidazoline compounds can exert profoundly detrimental effects on the growth and viability of clonal beta-cells but that these effects do not correlate with their binding affinity at imidazoline binding sites or alpha2-adrenoceptors.

Animals↗
PubMed2000

A circadian pacemaker in free-living chipmunks: essential for survival?

The importance of circadian timing was evaluated for 18 months from late-April 1997 through October 1998 in a high-density population of free-living eastern chipmunks, Tamias striatus, at a 4-ha forest site in the Allegheny Mountains. Included in the radiocollared field group were 30 chipmunks with supra-chiasmatic nucleus-targeted lesions, 24 surgical controls, and 20 intact controls. An additional 17 chipmunks were used in a laboratory study as lesion-calibration controls to correlate degree of circadian arrhythmicity with extent of supra-chiasmatic nucleus deletion. Survival was documented in the field by daily radio tracking and by regular trapping censuses except during winter hibernation. A significantly higher proportion of supra-chiasmatic nucleus-lesioned than surgical control chipmunks or intact controls were killed by weasel predation during the first 80 days after repatriation. A 28-h continuous census found no surface activity of any chipmunks during hours of darkness. However, episodes of nocturnal movement were detected within the permanent dens by radio telemetric data logging, especially in supra-chiasmatic nucleus-lesioned animals. Excavation and mapping of six chipmunk burrow systems aided in the interpretation of the telemetric activity data. Nighttime restlessness of supra-chiasmatic nucleus-lesioned animals may have acted as a clue to the predator for locating its prey.

Animals↗
PubMed2000

DEMS - a second generation diabetes electronic management system.

Diabetes electronic management system (DEMS) is a component-based client/server application, written in Visual C++ and Visual Basic, with the database server running Sybase System 11. DEMS is built entirely with a combination of dynamic link libraries (DLLs) and ActiveX components - the only exception is the DEMS.exe. DEMS is a chronic disease management system for patients with diabetes. It is used at the point of care by all members of the diabetes team including physicians, nurses, dieticians, clinical assistants and educators. The system is designed for maximum clinical efficiency and facilitates appropriately supervised delegation of care. Dispersed clinical sites may be supervised from a central location. The system is designed for ease of navigation; immediate provision of many types of automatically generated reports; quality audits; aids to compliance with good care guidelines; and alerts, advisories, prompts, and warnings that guide the care provider. The system now contains data on over 34000 patients and is in daily use at multiple sites.

Diabetes Mellitus↗
PubMed2000

Anti-beta2-glycoprotein I (GPI) autoantibodies, annexin V binding and the anti-phospholipid syndrome.

We examined the role of autoantibodies to beta2-GPI and prothrombin (PT) in the inhibition of annexin V binding to cardiolipin (CL) and the association with clinical manifestations of the anti-phospholipid syndrome (APS). Plasma samples from 59 patients with anti-phospholipid (aPL) antibodies were studied. Affinity purification of total IgG and IgG anti-ss2-GPI antibodies was performed using staphylococcal protein A and phospholipid liposomes. Annexin V binding to CL was significantly inhibited by 31/59 (53%) aPL+ plasma samples. There was a significant association between annexin V inhibition and elevated levels of IgG anti-cardiolipin (aCL) (r = -0.62; P < 0.001), IgG anti-ss2-GPI (r = -0.67; P < 0. 001) and a weaker association with lupus anti-coagulant (r = -0.27; P = 0.05). There was no association with other isotypes of aCL and anti-ss2-GPI or with anti-PT of any isotype. In patients with clinical manifestations of the APS there were higher levels of IgG aCL (median (range) Z score): 10.0 (0-17.6) versus 5.0 (0-16.1); P = 0.03), IgG anti-ss2-GPI (4.5 (0-11.3) versus 0.9 (0-9.7); P = 0.02) and greater inhibition of annexin V binding to CL (-3.4 (-11.4-0.6) versus -1.1 (-10.8-1.2); P = 0.22). Odds ratios for the laboratory assays and the presence of clinical manifestations of the APS varied between 0.38 and 4.16, with the highest values for IgG aCL (4.16), IgG anti-ss2-GPI (3.28) and annexin V inhibition (2.85). Additional experiments with affinity-purified IgG antibodies indicated that inhibition of annexin V binding was dependent upon the concentration of ss2-GPI and anti-ss2-GPI antibodies. These results indicate that inhibition of annexin V binding to procoagulant phospholipid surfaces is dependent upon anti-ss2-GPI antibodies and suggest a role for annexin V in the pathogenesis of the APS.

Annexin A5↗
PubMed2000

Towards an optimal model for community-based diabetes care: design and baseline data from the Mayo Health System Diabetes Translation Project.

The objective of the Mayo Health System Diabetes Translation Project is to assess the impact of three different models of care on the overall quality of diabetes care in the community. The unit of study is the primary care practice with a different model of care implemented at each of three sites. The design incorporates a comparison of a diabetes guideline implementation team initiative (Practice model A), a guideline initiative combined with clinical use of a Diabetes Electronic Management System (DEMS) by primary care providers (Practice model B) and a guideline initiative combined with DEMS utilization combined with electronic review of DEMS patient encounters by an endocrinologist (Practice model C). Administrative data sets were used to define the patient population at each practice. Patients were designated as new, attending or non-attending based on their pattern of visits over the preceding 12 months. A random sample of 200 charts from attending patients at each site was audited at baseline for diabetes-related process and outcome measures. This audit will be repeated yearly during the 2 years of the project. Baseline data revealed significant differences across sites in adherence to certain key indicators of the quality of diabetes care including: frequency of documentation of eye examinations (19, 39 and 37% for sites A, B and C, respectively), haemoglobin A1c monitoring (64, 89 and 77%) and microalbumin monitoring (3, 15 and 6%). The interventions being assessed in this study include traditional (diabetes education; guideline implementation) and modern (DEMS; telemedicine specialist review) methods for improving the quality of diabetes care. In spite of variation in baseline quality indicators, the setting and design should lead to broad applicability of the results and help determine an optimal model of diabetes care in the community.

Community Health Services↗
PubMed2000

Pharmacodynamics of warfarin in cats.

The overall purpose of this study was to evaluate the pharmacodynamic response to warfarin in cats. The specific aim was to determine if a log-linear indirect response model (Nagashima et al., 1969) used to describe the in vivo effect of warfarin in humans could be applied to cats. The pharmacokinetics of racemic warfarin were described using a non-compartmental approach. The relationship between prothrombin complex activity (PCA) and normalized prothrombin time (PTR) was defined for feline plasma under our experimental conditions, and determined to be: %PCA=12.38+648 e-PTR/0.492. These data were then integrated and used to predict the warfarin dose associated with therapeutic anti-coagulation defined as an International Normalized Ratio (INR) of 2.0-3.0. The maximum prothrombinopenic response to warfarin in cats after a single intravenous dose of 0.5 mg/kg occurred at 24-48 h. Pharmacodynamic modeling suggested that each cat had a narrow therapeutic range of the steady-state concentration of total warfarin required to appropriately block prothrombin complex synthesis (median: 265.2-358.7 ng/mL). The median daily dose range predicted to yield therapeutic concentrations of warfarin was 0.061-0.088 mg/kg per day. Wide inter-individual variations in both pharmacokinetics and pharmacodynamic response suggest that a more optimal dosing of warfarin may be possible with the development of individual pharmacokinetic/pharmacodynamic algorithms, analogous to those currently employed in human patients.

Animals↗
PubMed2000

Plasma pharmacokinetics of warfarin enantiomers in cats.

The purpose of this study was to determine the dispositions of S-warfarin and R-warfarin in normal cats following intravenous and oral administrations of racemic warfarin. Citrated blood samples were collected from 10 cats prior to and at times 5, 15, and 30 min, 1, 2, 3, 4, 5, 6, 12, 24, 36, 48, 72, 96, and 120 h following a single intravenous bolus of 0.5 mg/kg of racemic warfarin. After a 21-day washout period, samples were then similarly collected in three groups of four cats for 120 h following oral administration of 0.1, 0.25, and 0.5 mg/kg racemic warfarin. S-warfarin and R-warfarin were detected using a high-performance liquid chromatography assay validated for cat plasma. Drug concentration-time curves were subjected to non-compartmental analysis. Median pharmacokinetic parameters associated with the intravenous administration of 0.5 mg/kg racemic warfarin were as follows: t1/2 (S:28.2, R:18.3 h), area under the plasma concentration-time curve (AUC; S:33.0, R:24.6 h*microg/mL), area under the moment curve (AUMC; S:1889, R:527.8 h*h*microg/mL), and mean residence time (MRT; S:38.7, R:20.9 h). For each parameter, S-warfarin was significantly different from R-warfarin (P<0.05). Warfarin was absorbed rapidly after oral administration, and the dosage did not affect the time to maximum concentration (S:0.87, R:0.75 h). Oral dosage significantly influenced maximum plasma concentration (ng/mL, S:1267, R:1355 at 0.5 mg/kg; S:614.9, R:679.4 at 0.25 mg/kg; S:250.5, R:367.6 at 0.1 mg/kg), AUC (h*microg/mL, S:45.12, R:30.91 at 0.5 mg/kg; S:22.98:, R:18.99 at 0.25 mg/kg; S:3.922, R:3.570 at 0.1 mg/kg) and AUMC (h*h*microg/mL, S:2135, R:1062 at 0.5 mg/kg; S:943.1, R:599.9 at 0.25 mg/kg; S:132.2, R:59.03 at 0.1 mg/kg), but not t1/2 (S:23.5, R:11.6 h) nor MRT (S:26.3, R:13.5 h). Both warfarin enantiomers were highly (>96.5%) protein-bound. Quantitation of the warfarin content in commercially available tablets indicated an unequal distribution of the drug throughout the tablet.

Administration, Oral↗
PubMed2000

Rosiglitazone prevents the onset of hyperglycaemia and proteinuria in the Zucker diabetic fatty rat.

AIM: To investigate the potential of rosiglitazone, a highly potent agonist at the nuclear peroxisome proliferator activated receptor-gamma (PPAR-gamma), to prevent the development of diabetes in the Zucker diabetic fatty (ZDF) rat or to ameliorate the condition at a later stage of the disease. METHODS: Rosiglitazone (10 micromol/kg body weight daily) was given via the diet to ZDF rats from aged 6 weeks, before the onset of hyperglycaemia (Prevention group), or from aged 21 weeks after hyperglycaemia and proteinuria were established (Intervention group). Untreated ZDF rats and age-matched Zucker lean rats (ZL) served as controls and the experiment was terminated when the animals were aged 28 weeks. RESULTS: Whilst the combined ZDF control and Intervention groups were already hyperglycaemic (14.6 +/- 1.6 vs. ZL 5.7 +/- 0.1 mmol/l, mean +/- s.e.m.; p < 0.05), glycosuric and polydipsic at aged 11 weeks, and thereafter had a declining plasma insulin concentration, rosiglitazone Prevention treatment maintained normoglycaemia even at aged 27 weeks (3.7 +/- 0.3 mmol/l vs. ZL 3.0 +/- 0.3 mmol/l; NS). Intervention treatment at aged 21 weeks, however, failed to ameliorate the diabetes. These functional data were supported by determinations of pancreatic insulin content (microg/mg tissue as follows: ZL, 43.1 +/- 3.9; ZDF control (28 weeks) + ZDF Intervention control (21 weeks), 6.0 +/- 0.8; Prevention, 63.6 +/- 15.8; Intervention, 6.2 +/- 0.9) and by morphological, immunohistochemical and electron microscopical examination of pancreata at the end of the study. Thus, islets from rosiglitazone Prevention rats were similar to ZL rats, whereas ZDF controls and Intervention rats exhibited islets depleted of insulin, with a disorganized architecture and an ultrastructure indicative of work hypertrophy. ZDF control rats and Intervention rats, though not rosiglitazone Prevention rats, also exhibited marked proteinuria, indicative of renal glomerular damage. CONCLUSIONS: Our results demonstrate that in ZDF rats, rosiglitazone prevents the progression from insulin resistance to overt diabetes. These data provide a rationale for investigating whether treatment with rosiglitazone of patients with early signs of perturbed glucose metabolism (e.g. impaired fasting glucose (IGT)) may prevent the progression to type 2 diabetes and its associated complications.

Aging↗
PubMed2000

Differential baroreflex control of heart rate in sedentary and aerobically fit individuals.

PURPOSE: We compared arterial, aortic, and carotid-cardiac baroreflex sensitivity in eight average fit (maximal oxygen uptake, VO2max = 42.2+/-1.9 mL x kg(-1) x min(-1)) and eight high fit (VO2max = 61.9+/-2.2 mL x kg(-1) x min(-1)) healthy young adults. METHODS: Arterial and aortic (ABR) baroreflex functions were assessed utilizing hypo- and hyper-tensive challenges induced by graded bolus injections of sodium nitroprusside (SN) and phenylephrine (PE), respectively. Carotid baroreflex (CBR) sensitivity was determined using ramped 5-s pulses of both pressure and suction delivered to the carotid sinus via a neck chamber collar, independent of drug administration. RESULTS: During vasoactive drug injection, mean arterial pressure (MAP) was similarly altered in average fit (AF) and high fit (HF) groups. However, the heart rate (HR) response range of the arterial baroreflex was significantly attenuated (P < 0.05) in HF (31+/-4 beats x min(-1)) compared with AF individuals (46+/-4 beats x min(-1)). When sustained neck suction and pressure were applied to counteract altered carotid sinus pressure during SN and PE administration, isolating the ABR response, the response range remained diminished (P < 0.05) in the HF population (24+/-3 beats x min(-1)) compared with the AF group (41+/-4 beats x min(-1)). During CBR perturbation, the HF (14+/-1 beats-min(-1)) and AF (16+/-1 beats-min(-1)) response ranges were similar. The arterial baroreflex response range was significantly less than the simple sum of the CBR and ABR (HF, 38+/-3 beats x min(-1) and AF, 57+/-4 beats x min(-1)) in both fitness groups. CONCLUSIONS: These data confirm that reductions in arterial-cardiac reflex sensitivity are mediated by diminished ABR function. More importantly, these data suggest that the integrative relationship between the ABR and CBR contributing to arterial baroreflex control of HR is inhibitory in nature and not altered by exercise training.

Baroreflex↗
PubMed2000

Conserved surface-exposed K/R-X-K/R motifs and net positive charge on poxvirus complement control proteins serve as putative heparin binding sites and contribute to inhibition of molecular interactions with human endothelial cells: a novel mechanism for evasion of host defense.

Vaccinia virus complement control protein (VCP) has been shown to possess the ability to inhibit both classical and alternative complement pathway activation. The newly found ability of this protein to bind to heparin has been shown in previous studies to result in uptake by mast cells, possibly promoting tissue persistence. It has also been shown to reduce chemotactic migration of leukocytes by blocking chemokine binding. In addition, this study shows that VCP-through its ability to bind to glycosaminoglycans (heparin-like molecules) on the surface of human endothelial cells-is able to block antibody binding to surface major histocompatibility complex class I molecules. Since heparin binding is critical for many functions of this protein, we have attempted to characterize the molecular basis for this interaction. Segments of this protein, generated by genetic engineering of the DNA encoding VCP into the Pichia pastoris expression system, were used to localize the regions with heparin binding activity. These regions were then analyzed to more specifically define their properties for binding. It was found that the number of putative binding sites (K/R-X-K/R), the overall positive charge, and the percentage of positively charged amino acids within the protein were responsible for this interaction.

Amino Acid Motifs↗
PubMed2000

Forearm muscle metabolism studied using (31)P-MRS during progressive exercise to fatigue after Acz administration.

The effects of acetazolamide (Acz)-induced carbonic anhydrase inhibition (CAI) on muscle intracellular thresholds (T) for intracellular pH (pH(i)) and inorganic phosphate-to-phosphate creatine ratio (P(i)/PCr) and the plasma lactate (La(-)) threshold were examined in nine adult male subjects performing forearm wrist flexion exercise to fatigue. Exercise consisted of raising and lowering (1-s contraction, 1-s relaxation) a cylinder whose volume increased at a rate of 200 ml/min. The protocol was performed during control (Con) and after 45 min of CAI with Acz (10 mg/kg body wt iv). T(pH(i)) and T(P(i)/PCr), determined using (31)P-labeled magnetic resonance spectroscopy (MRS), were similar in Acz (722 +/- 50 and 796 +/- 75 mW, respectively) and Con (855 +/- 211 and 835 +/- 235 mW, respectively). The pH(i) was similar at end-exercise (6.38 +/- 0.10 Acz and 6.43 +/- 0.22 Con), but pH(i) recovery was slowed in Acz. In a separate experiment, blood was sampled from a deep arm vein at the elbow for determination of plasma lactate concentration ([La(-)](pl)) and T(La(-)). [La(-)](pl) was lower (P < 0.05) in Acz than Con (3.7 +/- 1.7 vs. 5.0 +/- 1.7 mmol/l) at end-exercise and in early recovery, but T(La(-)) was higher (1,433 +/- 243 vs. 1,041 +/- 414 mW, respectively). These data suggest that the lower [La(-)](pl) seen with CAI was not due to a delayed onset or rate of muscle La(-) accumulation but may be related to impaired La(-) removal from muscle.

Acetazolamide↗
PubMed2000

Gross morphology and topography of the adult intestinal tract of the tilapian fish, Oreochromis niloticus L.

The intestinal tract of the Nile tilapia, Oreochromis niloticus L., follows a complex course involving multiple loops and coils arranged in a previously undescribed form. From cranial to caudal, five principal regions were identified and designated as the hepatic loop (HL), proximal major coil (PMC), gastric loop (GL), distal major coil (DMC), and terminal segment (TS). The first four of these regions each possessed a reversal flexure and thus could be divided into proximal and distal limbs. Only the terminal segment was straight and undivided. The PMC and DMC were disposed in a spiral, cone-shaped mass (spiral intestine) - their proximal and distal limbs are thus designated as centripetal and centrifugal limbs. These spiral limbs were arranged with each successive limb nested internal to the previous one. Beginning from the stomach, the complete course of the gut including designations of the subdivisions of the major regions was as follows: proximal limb of the HL, distal limb of the HL, centripetal limb of the PMC, centrifugal limb of the PMC, proximal limb of the GL, distal limb of the GL, centripetal limb of the DMC, centrifugal limb of the DMC, and the TS. Though the topographical relations of the various gut loops permitted ready identification of each, external surface features were so similar among the segments that extirpated segments of gut could not be identified as to region of origin. The nesting of successive intestinal loops of the spiral intestine in this fish is novel among patterns previously described, and also among the more intricate of those that have been described.

Animals↗
PubMed2000

Autoimmune antiphospholipid antibodies and cryoglobulinemia.

In addition to their role in the thrombotic manifestations of the antiphospholipid syndrome (APS), autoimmune antiphospholipid (aPL) antibodies may also be responsible for direct injury to the blood vessel wall, although the mechanism is unclear. Cryoglobulinemia has been reported infrequently in patients with APS and is one potential means of blood vessel injury. The aim of the present study was to determine if autoimmune aPL antibodies and their target antigens contribute to the formation of cryoprecipitates. Cryoglobulins were identified and isolated from 5 of 8 patients with autoimmune aPL antibodies. Using identical concentrations of immunoglobulins isolated from matched sera and washed cryoprecipitates there was a significant enrichment (at least 100%) of aCL antibodies in the cryoprecipitates from 4 of 5 patients. This involved IgG, IgM and IgA isotypes with specificity for both beta2-glycoprotein I (GPI) and prothrombin (PT). The target antigens were detected in cryoprecipitates from all 5 aPL positive patients and in cryoprecipitates from 3 controls. These results suggest that anti-beta2-GPI and anti-PT antibodies in association with their target antigens are integrally involved in the formation of cryoprecipitates in patients with autoimmune aPL antibodies and provide insight into a potential mechanism for blood vessel injury.

Antibodies, Antiphospholipid↗