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Biomedical subjects

X Liu

Publications and source records attributed to X Liu.

At least 109 records · Page 6Linked to original sources

Comparative analysis of transcriptional profiles between two apoptotic pathways of light-induced retinal degeneration.

Light exposure can exacerbate the condition of a variety of human retinal diseases by increasing the rate of photoreceptor cell death. How light negatively affects photoreceptor cell survival is not yet fully understood. Previous studies involving light damage models have revealed two independent apoptotic pathways: low levels of light induce retinal degeneration in the arrestin -/- mouse via constitutive activation of the phototransduction cascade, whereas strong light exposure to the retina, such as in an albino eye, elicits photoreceptor cell death via activator protein (AP-1) induction. In order to better understand the initial gene expression changes underlying light damage, dark-reared arrestin -/- and albino BALB/c mice were exposed to constant white light (2000 lux), and their retinal morphology was assessed as a function of time. The expression profiles of retinal transcripts were then compared between dark-adapted and light-exposed arrestin -/-, pigmented wild-type and BALB/c mice at a time point when morphological changes were minimal. As expected, the dark-adapted samples showed little difference in expression pattern between the three genotypes. Among the genes differentially regulated by light in BALB/c, but not arrestin -/- retinas, were c-fos and other stress-induced early response genes. In both mouse models, a marked increase in expression of the bZIP family of transcription factors was observed. Our results show a select group of unique and overlapping sets of genes induced by light in the two mouse models. These expression changes may constitute the underlying initiating events leading to the two distinct mechanisms of light damage.

Animals↗

Apoptosis is caused by prolonged organ preservation and blocked by apoptosis inhibitor in experimental rat pancreatic grafts.

UNLABELLED: Apoptosis is a major mode of cell death after ischemia/reperfusion injury in several organs. The aims of this study were to evaluate apoptosis induction after different conditions of pancreas preservation and to investigate the impact of a caspase inhibitor on apoptosis induction in pancreatic grafts. METHODS: Inbred male Lewis rats served as donors and recipients. Apoptosis was detected using an in situ cell death detection kit and an apoptotic DNA ladder kit (Roche, Germany). An apoptotic index (AI) was defined as the number of apoptotic cells per field (400x) under a light microscope. The five groups included: group 1 (n = 5), normal pancreata; group 2 (n = 7), pancreata stored in University of Wisconsin (UW) solution (4 degrees C) for 6 hours (hr); group 3 (n = 7), pancreata preserved in UW solution (4 degrees C) for 18 hr; group 4 (n = 7), pancreata preserved in 0.9% saline (4 degrees C) for 6 hours; and group 5 (n = 5), pancreata preserved in 0.9% saline (4 degrees C) for 6 hours with Z-Asp-2,6-dichlorobenzoyloxymethylketone (caspase inhibitor) treatment. The pancreatic grafts in all experimental groups underwent a 2-hr period of reperfusion after transplantation. RESULTS: The results in this study showed that the AI was not significantly increased among pancreatic grafts in group 2 compared to group 1 (P >.05). However, AI in group 3 was significantly higher than that in group 2 (P <.05). The highest AI was observed in group 4. Interestingly, AI in group 5 was significantly lower than that in group 4 (P <.01), and not significantly different from group 1 (P >.05). Apoptotic DNA ladders were detected in the pancreatic grafts in group 2, 3, and 4, but not in group 1 and 5. CONCLUSIONS: Prolonged preservation of pancreata in cold UW solution induces a dramatic increase in apoptotic cell death among the pancreatic grafts following Tx. This observation may well be an important mechanism of graft damage. A caspase inhibitor might be useful to inhibit apoptosis induction in pancreatic grafts.

Adenosine↗

Islet autotransplantation combined with pancreatectomy for treatment of pancreatic adenocarcinoma: a case report.

Extensive pancreatectomy (EP) may increase the resection rate of pancreatic adenocarcinoma (PA). Unfortunately, EP often results in unstable diabetes. Recently, islet autotransplantation (auto-Tx) has offered the potential to prevent this metabolic disorder. Because of the fear of contamination of prepared islets by malignant cells, this procedure has so far not been used as a treatment for PA. We herein report a case of a 63-year-old nondiabetic patient who underwent EP combined with islet auto-Tx in an emergency operation following histologically proved R(0)-resection for PA (pT(3)pN(1)G(2)). Islets were isolated from the excised pancreas using a continuous digestion filtration device. The resultant preparation was injected into the portal vein. Owing to the moderate fasting hyperglycemia, postoperative exogenous insulin therapy was necessary (26 U/d). After discharge, the patient's daily insulin dose was gradually reduced. At 1-year follow-up the fasting C-peptide level was 0.66 ng/mL, and an oral glucose tolerance test (oGTT) and an intravenous (IV) glucagon stimulation (GS) showed functioning engrafted islets. The K-ras mutations were detected in the paraffin-embedded PA, but not in the prepared islets or in the peripheral blood. Computed tomographic (CT) imaging revealed neither local tumor recurrence nor liver metastases. At 2-year follow-up, the patient was on a balanced food regimen and gaining weight. Although he remains insulin-dependent (16 U/d), he is metabolically stable (HbA(1)(c) 5.9%). The fasting C-peptide level is 0.68 ng/mL. The peak value of C-peptide in response to oGTT was 0.92 ng/mL and to GS 0.89 ng/mL. At this time Ca19-9 and CEA are increased to 35.3 U/mL and 19.2 ng/mL, respectively. The patient died 2.5 years after operation owing to tumor recurrence. There was no evidence for liver metastases. We postulate that histologic evaluation (R(0)-resection) and detection of K-ras mutations may be useful techniques. However, islet auto-Tx after EP for adenocarcinoma should only be regarded for rescue therapy. Studies on strategies to exclude possible contamination of islet tissue with carcinoma cells are critically important.

Adenocarcinoma↗

Association between apolipoprotein CI HpaI polymorphism and sporadic Alzheimer's disease in Chinese.

OBJECTIVE: To investigate into the relationship of apolipoprotein CI (ApoCI) polymorphism with sporadic Alzheimer's disease (AD) in Chinese. SUBJECTS AND METHODS: A total of 257 AD patients and 242 age-matched elderly individuals were genotyped for the ApoCI HpaI and apolipoprotein E (ApoE) HhaI polymorphisms. RESULTS: The ApoCI A allele was associated with AD of moderate to severe dementia when patients were divided into two subgroups according to Clinical Dementia Rating scale, and the AA genotype was strongly associated with moderate to severe AD in ApoE epsilon4 allele carriers [odds ratio (OR) = 8.19, 95% confidential interval: 1.28-52.30, after adjusting for age and gender by logistic regression analysis], although in total no significant differences of allele or genotype frequency between patients and controls were found. CONCLUSION: The present study partially confirmed the previous findings, suggesting that the ApoCI A allele might contribute to the susceptibility to moderate to severe sporadic AD in Chinese.

Aged↗

Disorders of the blood-aqueous barrier after phacoemulsification in diabetic patients.

PURPOSE: To evaluate the function of the blood-aqueous barrier after phacoemulsification with implantation of a foldable intraocular lens (IOL) in diabetic patients. METHODS: All patients were enrolled from those scheduled for phacoemulsification with intraocular lens implantation in Zhongshan Ophthalmic Center Guangzhou from March 2002 to June 2002. The classification on diabetic retinopathy (DR) was based on the fundus examination after cataract surgery. The blood-aqueous barrier function was examined using the laser flare cell meter (Kowa FC-2000) preoperatively and on postoperative days 1, 7, 30, and 90 by an independent examiner who was masked to the DR classification. Patients were operated by one experienced surgeon as per standard clinical protocol and were provided the same postoperative medical care. A linear regression and Wilcoxon test were used for the analysis. RESULTS: A total of 112 patients were divided into three groups: patients without diabetic mellitus as normal control (n=56), diabetic patients without diabetic retinopathy (n=2), with nonproliferation diabetic retinopathy (NPDR) (n=37), and diabetic patients with proliferation diabetic retinopathy (PDR) (n=17). All patients were examined and successfully followed up for 3 months after cataract surgery. Aqueous flare mean photon counts in PDR, NPDR, and control eyes were 8.94+/-0.57, 7.03+/-0.27, and 6.94+/-0.34 before surgery and increased to 32.42+/-0.67, 26.07+/-0.83, 26.27+/-1.37 on the first day after surgery (P<0.05), then decreased to 19.86+/-0.78, 14.08+/-0.54 and 13.96+/-1.05 at 7 days after surgery (P<0.05), 13.24+/-0.29, 9.86+/-0.33, and 9.07+/-0.43 at 30 days after surgery (P<0.05); eventually, the counting decreased to 11.25+/-0.31, 7.24+/-0.67, and 7.16+/-0.27 at 90 days after surgery (P<0.05). Linear regression model suggested that other potential variables, such as age, sex, eye (left/right), phaco time, phaco energy, and hypertension were not related to the outcome. For patients without diabetes mellitus and diabetic patients with NPDR, highly statistically significant differences (P<0.05) were found between preoperative flare value and those measured on days 1, 7, and 30 after surgery, but no statistically significant differences (P>0.05) were found between the preoperative flare value and those measured on postoperative days 90. However, patients with PDR still had a higher flare value even on postoperative day 90. The patients with intraoperative iris prolapse had a higher flare value between days 1 and 7 postoperatively. CONCLUSION: Phacoemulsification with a foldable intraocular lens implantation affects the blood-aqueous barrier more severely in diabetic patients with PDR than patients with NPDR and nondiabetic patients.

Aged↗

Identification of a novel neuregulin 1 at-risk haplotype in Han schizophrenia Chinese patients, but no association with the Icelandic/Scottish risk haplotype.

To determine if neuregulin 1 (NRG1) is associated with schizophrenia in Asian populations, we investigated a Han Chinese population using both a family trio design and a case-control design. A total of 25 microsatellite markers and single nucleotide polymorphisms (SNPs) were genotyped spanning the 1.1 Mb NRG1 gene including markers of a seven-marker haplotype at the 5' end of the gene found to be in excess in Icelandic and Scottish schizophrenia patients. The alleles of the individual markers forming the seven marker at-risk haplotype are not likely to be causative as they are not in excess in patients in the Chinese population studied here. However using unrelated patients, we find a novel haplotype (HAP(China 1)), immediately upstream of the Icelandic haplotype, in excess in patients (11.9% in patients vs 4.2% in controls; P=0.0000065, risk ratio (rr) 3.1), which was not significant when parental controls were used. Another haplotype (HAP(China 2)) overlapping the Icelandic risk haplotype was found in excess in the Chinese (8.5% of patients vs 4.0% of unrelated controls; P=0.003, rr 2.2) and was also significant using parental controls only (P=0.0047, rr 2.1). A four-marker haplotype at the 3' end of the NRG1 gene, HAP(China 3), was found at a frequency of 23.8% in patients and 13.7% in nontransmitted parental haplotypes (P=0.000042, rr=2.0) but was not significant in the case-control comparison. We conclude that different haplotypes within the boundaries of the NRG1 gene may be associated with schizophrenia in the Han Chinese.

Asian People↗

Copasetic analysis: a framework for the blind analysis of microarray imagery.

From its conception, bioinformatics has been a multidisciplinary field which blends domain expert knowledge with new and existing processing techniques, all of which are focused on a common goal. Typically, these techniques have focused on the direct analysis of raw microarray image data. Unfortunately, this fails to utilise the image's full potential and in practice, this results in the lab technician having to guide the analysis algorithms. This paper presents a dynamic framework that aims to automate the process of microarray image analysis using a variety of techniques. An overview of the entire framework process is presented, the robustness of which is challenged throughout with a selection of real examples containing varying degrees of noise. The results show the potential of the proposed framework in its ability to determine slide layout accurately and perform analysis without prior structural knowledge. The algorithm achieves approximately, a 1 to 3 dB improved peak signal-to-noise ratio compared to conventional processing techniques like those implemented in GenePix when used by a trained operator. As far as the authors are aware, this is the first time such a comprehensive framework concept has been directly applied to the area of microarray image analysis.

Artificial Intelligence↗

17beta-estradiol prevents blood-brain barrier disruption induced by VEGF.

We performed this study to determine how pretreatment of the ovariectomized rats with 17beta-estradiol could affect blood-brain barrier disruption caused by the vascular endothelial growth factor (VEGF), an important mediator of vascular permeability. Ovariectomized female rats aged twelve to fourteen weeks were used in the study. A 500 micro g 17beta-estradiol 21-day release pellet was implanted in the 17beta-estradiol group, and a vehicle pellet was implanted in the control group 21 days before the experiments. We performed three craniotomies under isoflurane anesthesia to expose cerebral cortices. Normal saline, 10 (- 10)M and 10 (- 9)M VEGF patches were applied on each hole for 30 min. The transfer coefficient (Ki) of (14)C-alpha-amino isobutyric acid and volume of (3)H-dextran (70,000 dalton) distribution were determined to measure the degree of BBB disruption. Ki was increased by 108 % and 138 % with 10 (- 10)M and 10 (- 9)M VEGF respectively after VEGF application in the control group (p < 0.01). However, there was no significant increase in the Ki with the VEGF application in the 17beta-estradiol group, and their values were significantly lower than the corresponding data of the control group (10 (- 10)M: - 55 %, 10 (- 9)M: - 52 %, p <0.05). The volume of dextran distribution in the control group increased by 47 % with VEGF 10 (- 9)M (p < 0.05), whereas there was no significant change in the volume of dextran distribution with VEGF application in the 17beta-estradiol group and the volume was lower than the corresponding volume of the vehicle-treated control group (10 (- 10)M: - 34 %, 10 (- 9)M: -32 %, p < 0.05). In conclusion, our study demonstrated that chronic 17beta-estradiol treatment prevented BBB disruption induced by the VEGF in the ovariectomized rats.

Animals↗

Correlation of ph dependant equilibrium isotherms of heavy metal biosorption with a modified Freundlich model.

Equilibrium isotherms of heavy metal biosorption are commonly correlated with adsorption models such as the Freundlich model. On the other hand, the adsorption properties of heavy metal biosorption are strongly influenced by the solution pH of the biosorption system. Therefore, standard adsorption models are limited to the correlation of equilibrium isotherms under constant pH values. In this paper, a modified Freundlich model was developed for the correlation of pH dependent equilibrium isotherms of heavy metal biosorption. The model was based on the mechanism that the functional groups for heavy metal interactions are weakly acidic groups and the uptake capacities of the biomass are affected through the association and dissociation equilibrium between two apparent ionic forms. Both the standard and the modified Freundlich models were tested with isotherm data for Cd2+, Cu2+ and Ni2+ biosorption onto pre-treated biomass of marine alga Durvillaea potatorum under various solution pH values. Regression analyses indicated that the developed model correlated the experimental data well.

Adsorption↗

Effects of syndecan-1 and glypican on muscle cell proliferation and differentiation: implications for possible functions during myogenesis.

The heparan sulfate proteoglycans, syndecan-1 and glypican, are low-affinity receptors for fibroblast growth factor 2 (FGF2). Because FGF2 is a potent stimulator of skeletal muscle cell proliferation and a strong inhibitor of differentiation, it is likely that changes in syndecan-1 and glypican expression will affect myogenesis as both, in part, regulate FGF-dependent signaling. In the current study, expression vector constructs containing either syndecan-1 or glypican were transfected into turkey myogenic satellite cells resulting in the overexpression of these genes. The amount of expression of each of these genes was measured by semiquantitative reverse transcriptase polymerase chain reaction. The satellite cell cultures overexpressing syndecan-1 were unable to fuse to form multinucleated myotubes after differentiation was induced. The syndecan-1-transfected cells maintained a rounded morphology typical of cells during proliferation. In contrast, the satellite cells transfected with glypican formed larger myotubes. These results suggest that both syndecan-1 and glypican play pivotal, but different, roles in both muscle cell proliferation and differentiation.

Animals↗

The influence of selection for increased body weight and sex on pectoralis major muscle weight during the embryonic and posthatch periods.

Skeletal muscle development and growth results from a complex series of highly organized processes. To address how myogenesis was influenced by selection for increased BW and by sex, both sexes from a turkey line (F) selected only for increased 16-wk BW and its genetic control line (RBC2) were used. Pectoralis major muscle was isolated and weighed from 15 individuals of each sex of the F and RBC2 lines at 14, 16, 18, 20, and 24 d of embryonic development and at 1, 8, 12, and 16 wk of age posthatch. The F line had significantly heavier p. major muscle weights than the RBC2 line beginning at 16 d of embryonic development, and the magnitude of the line differences generally increased with age through 16 wk posthatch The p. major muscle was consistently heavier in males than in females, but the differences between sexes were significant only at 16, 18, and 24 d of embryonic development and at 8 wk posthatch. There was no significant interaction between line and sex for weight of the p. major muscle at any age. The results indicated that selection for increased 16-wk BW in the F line altered growth of the p. major muscle by 16 d of embryonic development and changes were similar for both sexes.

Animals↗

A group of related cDNAs encoding secreted proteins from Hessian fly [Mayetiola destructor (Say)] salivary glands.

A group of cDNAs has been isolated and characterized from Hessian fly [Mayetiola destructor (Say)] salivary glands. Members in this group appear to encode proteins with secretion signal peptides at the N-terminals. The mature putative proteins are small, basic proteins with calculated molecular weights that ranged from 8.5 to 10 kDa, and isoelectric points from 9.92 to 10.90. Sequence analysis indicated a strong selection for mutations that generate amino acid changes within the coding region. Northern blot analysis revealed that these genes are expressed only in the first instar larvae, a critical stage that determines if the interaction between a specific Hessian fly biotype and a specific wheat cultivar is compatible. Genomic analysis demonstrated that multiple copies of similar genes are clustered within a short region on chromosome 2A. This is the same arm in which two avirulence genes have been mapped.

Amino Acid Sequence↗

Identified spinal motoneurons of young rats possess nicotinic acetylcholine receptors of the heteromeric family.

The aim of the present study was to determine whether, in young rats, spinal motoneurons possess functional nicotinic acetylcholine receptors. Motoneurons were identified either by retrograde labelling or by choline acetyltransferase immunohistochemistry. Whole-cell recordings were performed in spinal cord slices cut at the lumbar level. In voltage clamp, acetylcholine evoked a rapidly activating inward current. In current clamp, it depolarized the motoneuron membrane and induced action potential firing. The acetylcholine-evoked current was strongly reduced by d-tubocurarine or dihydro-beta-erythroidine, broad spectrum nicotinic antagonists, but was almost insensitive to methyllycaconitine, a nicotinic antagonist selective for receptors containing the alpha7 subunit. Moreover, exo-2-(2-pyridyl)-7-azabicyclo[2.2.1]heptane, an alpha7-specific agonist, was without effect. In young animals, light-microscopic autoradiography showed that in the central grey matter all laminae were intensely and equally labelled by [3H]epibatidine. A dense [125I]-alpha-bungarotoxin binding was also found in all laminae, with slightly lower levels in the superficial layers of the dorsal horns and in the ventral part of the grey matter. In adults, the density of [3H]epibatidine binding sites was much lower in the entire grey matter, except in layer 2 of the dorsal horn, and [125I]-alpha-bungarotoxin binding sites were present only in some selected areas. Our data indicate that spinal motoneurons possess functional nicotinic receptors of the heteromeric type and suggest that nicotinic cholinergic transmission may play a significant role in the developing spinal cord.

Acetylcholine↗

Coupling of functional gene diversity and geochemical data from environmental samples.

Genomic techniques commonly used for assessing distributions of microorganisms in the environment often produce small sample sizes. We investigated artificial neural networks for analyzing the distributions of nitrite reductase genes (nirS and nirK) and two sets of dissimilatory sulfite reductase genes (dsrAB1 and dsrAB2) in small sample sets. Data reduction (to reduce the number of input parameters), cross-validation (to measure the generalization error), weight decay (to adjust model parameters to reduce generalization error), and importance analysis (to determine which variables had the most influence) were useful in developing and interpreting neural network models that could be used to infer relationships between geochemistry and gene distributions. A robust relationship was observed between geochemistry and the frequencies of genes that were not closely related to known dissimilatory sulfite reductase genes (dsrAB2). Uranium and sulfate appeared to be the most related to distribution of two groups of these unusual dsrAB-related genes. For the other three groups, the distributions appeared to be related to pH, nickel, nonpurgeable organic carbon, and total organic carbon. The models relating the geochemical parameters to the distributions of the nirS, nirK, and dsrAB1 genes did not generalize as well as the models for dsrAB2. The data also illustrate the danger (generating a model that has a high generalization error) of not using a validation approach in evaluating the meaningfulness of the fit of linear or nonlinear models to such small sample sizes.

Bacteria↗

Methotrexate loaded SAE coated coronary stents reduce neointimal hyperplasia in a porcine coronary model.

OBJECTIVE: To evaluate the effect of stent based methotrexate delivery on neointimal hyperplasia. METHODS: Stainless steel coronary stents and biological polymer coated (SAE) stents were randomly implanted in coronary arteries of pigs with a stent to artery ratio of 1.1:1. The pigs were killed after five days (10 stents) or four weeks (20 stents). Second, stainless steel coronary stents were dip coated in a 10 mg/ml methotrexate-SAE polymer solution, resulting in a total load of 150 microg methotrexate/stent. SAE coated stents and methotrexate loaded stents were randomly implanted in porcine coronary arteries with a stent to artery ratio of 1.2:1 and followed up to four weeks. RESULTS: SAE coated stents and bare stents elicited a similar tissue response at five days. At four weeks, neointimal hyperplasia induced by the coated stents was less pronounced than with the bare stents (1.32 (0.66) v 1.73 (0.93) mm2, p > 0.05). In vitro drug release studies showed that 50% of the methotrexate was released in 24 hours, and all drug was released within four weeks. No impact on vascular smooth muscle cell proliferation or viability was observed in in vitro cell cultures. At four weeks the arteries with methotrexate loaded stents had decreased peristrut inflammation and neointimal hyperplasia (1.22 (0.34) v 2.25 (1.28) mm2, p < 0.01). CONCLUSIONS: SAE coating had an excellent biocompatibility with vascular tissue. Stent based delivery of methotrexate in the SAE coating effectively reduced neointimal hyperplasia in a porcine coronary stent model, potentially due to reduced peristrut inflammation.

Animals↗

Thrombin induces collagen gel contraction partially through PAR1 activation and PKC-epsilon.

The ability of fibroblasts to contract three-dimensional collagen gels has been used as an in vitro model of the tissue contraction which characterises both normal repair and fibrosis. Among its actions, thrombin can activate the protease-activated receptor (PAR)1 and, thereby, stimulate inflammation and repair. The current study evaluated whether thrombin could stimulate fibroblast-mediated collagen gel contraction by activating PAR1 and whether its downstream signalling depends on protein kinase C (PKC)-epsilon. Human foetal lung fibroblasts (HFL-1) were cultured in three-dimensional collagen gels and the area of the gels was measured by image analyser. Both thrombin and TFLLR, a selective PAR1 agonist, stimulated collagen gel contraction mediated by HFL-1. After RNA interference-mediated PAR1 knockdown in HFL-1, both thrombin and the PAR1 agonist-induced gel contraction were partially inhibited (by 22.4+/-2.2% and 17.6+/-5.6%, respectively). The gel contraction stimulated by thrombin was also reduced by a nonspecific PKC inhibitor and a calcium-independent PKC-epsilon inhibitor. Both thrombin and TFLLR significantly increased PKC-epsilon activity, and this effect was blocked by PAR1 knockdown. Thrombin stimulates collagen gel contraction at least partially through activation of protease-activated receptor 1 and protein kinase C-epsilon, and may contribute to tissue remodelling in inflammatory airway and lung diseases.

Analysis of Variance↗

Intrauterine fetal death in mice caused by cytomegalovirus-derived peptide induced aPL antibodies.

Immunization of mice with beta2 glycoprotein I (beta2GPI) and also with GDKV, a synthetic peptide representing the phospholipid (PL)-binding site of beta2GPI, induced pathogenic aPL antibodies that bind and activate endothelial cells, enhanced thrombus formation and caused fetal death in pregnant mice. TIFI is a PL-binding peptide spanning the Thr101-Thr120 of ulb0-hcmva from human cytomegalovirus (CMV), which shares structural similarity with the PL-binding site of beta2GPI. Immunization with this peptide induced pathogenic aPL and anti-beta2GPI antibodies in mice. These antibodies activated endothelial cells and enhanced thrombus formation in vivo, but whether these antibodies cause fetal death in mice is not known. The objective of this study was to examine the effects of these antibodies on pregnancy outcome in mice. Two groups of pregnant BALB/c mice were injected with either hybridoma supernatant containing D3/AC10, a CMV-peptide-induced monoclonal aPL, at days four, eight and 12 of the pregnancy, 100 microg per mouse (study group) or with culture media alone (control group). The litter size was significantly smaller in the study group (4.80 +/- 1.15 versus 7.28 +/- 0.18, t = - 2.526, P < 0.03). In conclusion, aPL induced by CMV peptides may have pathogenic properties similar to human autoimmune aPL. These findings further support the hypothesis that at least in some patients with APS, pathogenic aPL antibodies may be generated by immunization with CMV products during incidental exposure to the virus via a molecular mimicry mechanism.

Animals↗