Search PubMed⌕ Search

Biomedical subjects

D Wendt

Publications and source records attributed to D Wendt.

At least 19 recordsLinked to original sources

Engineering of osteoinductive grafts by isolation and expansion of ovine bone marrow stromal cells directly on 3D ceramic scaffolds.

In this work, we investigated whether osteoinductive constructs can be generated by isolation and expansion of sheep bone marrow stromal cells (BMSC) directly within three-dimensional (3D) ceramic scaffolds, bypassing the typical phase of monolayer (2D) expansion prior to scaffold loading. Nucleated cells from sheep bone marrow aspirate were seeded into 3D ceramic scaffolds either by static loading or under perfusion flow and maintained in culture for up to 14 days. The resulting constructs were exposed to enzymatic treatment to assess the number and lineage of extracted cells, or implanted subcutaneously in nude mice to test their capacity to induce bone formation. As a control, BMSC expanded in monolayer for 14 days were also seeded into the scaffolds and implanted. BMSC could be isolated and expanded directly in the 3D ceramic scaffolds, although they proliferated slower than in 2D. Upon ectopic implantation, the resulting constructs formed a higher amount of bone tissue than constructs loaded with the same number of 2D-expanded cells. Constructs cultivated for 14 days generated significantly more bone tissue than those cultured for 3 days. No differences in bone formation were found between samples seeded by static loading or under perfusion. In conclusion, the culture of bone marrow nucleated cells directly on 3D ceramic scaffolds represents a promising approach to expand BMSC and streamline the engineering of osteoinductive grafts.

Animals↗

Comparison of the established standard complement-dependent cytotoxicity and flow cytometric crossmatch assays with a novel ELISA-based HLA crossmatch procedure.

The detection of donor-specific anti-HLA antibodies by standard procedures such as complement-dependent cytotoxicity assay (CDC) or flow cytometric (FACS) analysis is limited by its low sensitivity and the quality of the donor cells. Therefore, an ELISA-based technique was employed using solid phase-immobilized monoclonal antibodies to capture HLA class I or class II molecules of the donor, respectively. In this HLA class I and class II antibody monitoring system (AMS) the donor-specific anti-HLA antibodies from the sera of recipients bind to the HLA molecules of the donor which have been immobilized by monoclonal antibodies (mAb) recognizing non-polymorphic epitopes. Upon binding of donor-specific anti-HLA antibodies they are recognized by secondary enzyme-conjugated anti-human immunoglobulin (Ig) antibodies. A newly established modification of the standard protocol allows the differentiation between bound antibodies of the IgG and IgM isotype. Furthermore, this assay was adapted for investigating small amounts of solid tissue of donors from whom no other cells (e.g. from blood) were available. We here provide an overview of the classical crossmatch methods with their advantages and limits. In addition, the design of the novel AMS-ELISA is described in terms of quality and sensitivity of the approach using exemplary cases of different application. The selected cases show that the AMS-ELISA represents a valuable tool for the post-transplantation monitoring of donor-specific anti-HLA antibodies during reaction crisis, after transfusion reactions and in particular cases of tissue transplantations lacking single cells.

Antibodies, Monoclonal↗

Structural characterization and reliable biomechanical assessment of integrative cartilage repair.

Structural and functional characterization of integrative cartilage repair in controlled model systems can play a key role in the development of innovative strategies to improve the long-term outcome of many cartilage repair procedures. In this work, we first developed a method to reproducibly generate geometrically defined disk/ring cartilage composites and to remove outgrown fibrous layers which can encapsulate cartilaginous tissues during culture. We then used the model system to test the hypothesis that such fibrous layers lead to an overestimation of biomechanical parameters of integration at the disk/ring interface. Transmission electron microscopy images of the composites after 6 weeks of culture indicated that collagen fibrils in the fibrous tissue layer were well integrated into the collagen network of the cartilage disk and ring, whereas molecular bridging between opposing disk/ring cartilage surfaces was less pronounced and restricted to regions with narrow interfacial regions (< 2 microm). Stress-strain profiles generated from mechanical push-out tests for composites with the layers removed displayed a single and distinct peak, whereas profiles for composites with the layers left intact consisted of multiple superimposed peaks. As compared to composites with removed layers, composites with intact layers had significantly higher adhesive strengths (161+/-9 vs. 71+/-11 kPa) and adhesion energies (15.0+/-0.7 vs. 2.7+/-0.4 mJ/mm2). By combining structural and functional analyses, we demonstrated that the outgrowing tissue formed during in vitro culture of cartilaginous specimens should be eliminated in order to reliably quantify biomechanical parameters related to integrative cartilage repair.

Adhesiveness↗

Deleterious effects of oxygen during extracorporeal circulation for the microcirculation in vivo.

OBJECTIVE: Clinical complications arising from extracorporeal circulation (ECC) have been linked to disturbances in the microcirculation. Hyperoxia, a mainstay of supportive treatment, is clinically used for a variety of pathological states. In previous in vivo animal experiments we found increased leukocyte/endothelial (L/E) cell interaction following ECC due to oxygen derived free radicals. This study was carried out to investigate the link between arterial pO2 during ECC and the potential damage to the microcirculation, supposedly caused by oxygen derived radicals. METHODS: Intravital fluorescence microscopy was used on the dorsal skinfold chamber preparation in syrian golden hamsters. ECC was introduced via a micro-rollerpump (0.7 ml/min) and a 60 cm silicon tube (1 mm inner diameter) shunted between the carotid artery and the jugular vein after application of 300 IE Heparin/kg/bw. Experiments were performed in chronically instrumented, awake animals (age: 10-14 weeks, weight: 65-75 g). Control inspired room air, experimental group 1 inspired 100% oxygen, group 2 received 100% oxygen and 2000 IE of Heparin i.v. (n=7/group), that releases endothelial bound superoxide dismutase, a natural scavenger of oxygen derived free radicals in the hamster. RESULTS: Normobaric inhalation of 100% oxygen increased arterial pO2 from 64+/-8.1 mmHg to 512+/-124 mmHg (P<0.05 vs. baseline). ECC under 100% oxygen reduced functional capillary density (FCD) to 70% of baseline values 8 h after ECC (P<0.05). Adherent leukocytes in postcapillary venules and arterioles increased significantly (P<0.05). 2000 IE Heparin prevented the reduction in FCD and decreased the number of adherent leukocytes. CONCLUSIONS: Reduction in FCD, increased leukocyte adherence to the microvascular endothelium of postcapillary venules and arterioles under hyperoxia compared to ECC under room air conditions, demonstrates harmful effects of oxygen during ECC in vivo. A high dose of Heparin enhances functional capillary density, thus attenuating the microvascular dysfunction/damage in the period after ECC.

Animals↗

Oscillating perfusion of cell suspensions through three-dimensional scaffolds enhances cell seeding efficiency and uniformity.

We developed a bioreactor for automated cell seeding of three-dimensional scaffolds by continuous perfusion of a cell suspension through the scaffold pores in oscillating directions. Using quantitative biochemical and image analysis techniques, we then evaluated the efficiency and uniformity of perfusion seeding of Polyactive foams as compared to conventional static and spinner flask methods. Finally, we assessed the efficacy of the perfusion seeding technique for different scaffolds and cell types. Perfusion seeding of chondrocytes into Polyactive foams resulted in "viable cell seeding efficiencies," defined as the percentages of initially loaded cells that were seeded and remained viable, that were significantly higher (75 +/- 6%) than those by static (57% +/- 5%) and spinner flask seeding (55% +/- 8%). In addition, as compared to static and spinner flask methods, cells seeded by perfusion were respectively 2.6-fold and 3.8-fold more uniformly distributed and formed more homogeneously sized cell clusters. Chondrocytes seeded by perfusion into Hyaff-11 nonwoven meshes were 26% and 63%, respectively, more uniformly distributed than following static and spinner flask seeding. Bone marrow stromal cells seeded by perfusion into ChronOS porous ceramics were homogeneously distributed throughout the scaffold volume, while following the static method, cells were found only near the top surface of the ceramic. In summary, we demonstrated that our cell seeding perfusion bioreactor generated constructs with remarkably uniform cell distributions at high efficiencies, and was effective for a variety of scaffolds and different mesenchymal cell types.

Animals↗

Dynamic compression of cartilage constructs engineered from expanded human articular chondrocytes.

Recent works have shown that mechanical loading can alter the metabolic activity of chondrocytes cultured in 3D scaffolds. In this study we determined whether the stage of development of engineered cartilaginous constructs (expanded adult human articular chondrocytes/Polyactive foams) regulates the effect of dynamic compression on glycosaminoglycan (GAG) metabolism. Construct maturation depended on the culture time (3-14 days) and the donor (4 individuals). When dynamic compression was subsequently applied for 3 days, changes in GAG synthesized, accumulated, and released were significantly positively correlated to the GAG content of the constructs prior to loading, and resulted in stimulation of GAG formation only in the most developed tissues. Conversely, none of these changes were correlated with the expression of collagen type II mRNA, indicating that the response of chondrocytes to dynamic compression does not depend directly upon the stage of cell differentiation, but rather on the extracellular matrix surrounding the cells.

Cartilage, Articular↗

MLC quality assurance techniques for IMRT applications.

Intensity modulated radiotherapy (IMRT) requires extensive knowledge of multileaf collimator (MLC) leaf positioning accuracy, precision, and long-term reproducibility. We have developed a technique to efficiently measure the absolute position of each MLC leaf, over the range of leaf positions utilized in IMRT, based on dosimetric information. A single radiographic film was exposed to 6 MV x-rays for twelve exposures: one open field with a radio-opaque marker tray present, and eleven fields (1 x 28 cm strips via 1 cm gaps between opposed leaf pairs) separated by 2 cm center to center. The process was repeated while varying direction of leaf travel; each film was digitized using a commercial film dosimetry system. The digital images were manipulated to remove translation and rotation of the film data with respect to the collimator coordinate system by extraction of radiation dose profiles perpendicular to the MLC leaf motion and measuring the center of the x-ray leakage between leaves. Radiation dose profiles in the direction of leaf motion were acquired through the center of each leaf pair (leaves 2-28), which provided leaf position information every 2 cm with 0.2 mm precision. Nine separate leaf reproducibility studies over a 90 day period which evaluated 600 measurement points on each film show 0.3 mm precision for 95% confidence, while hysteresis studies show 0.5 mm precision. Absolute leaf position error measurements demonstrated a radial dependence, with a maximum of 1.5 mm at 16.4 cm from central axis, due to rotational error at calibration. Recalibration of the MLC leaves based utilizing this tool yields absolute leaf position measurements where 91.5% of all leaves/positions were within 0.5 mm, with a mean error of 0.1 mm and a maximum error less than 1.0 mm.

Equipment Design↗

A polymorphism, L162V, in the peroxisome proliferator-activated receptor alpha (PPARalpha) gene is associated with lower body mass index in patients with non-insulin-dependent diabetes mellitus.

This study examined the effect a polymorphism (L162V) in the gene for peroxisome proliferator activated receptor (PPAR) alpha in the development of non-insulin-dependent diabetes mellitus (type 2 DM), obesity and hyperlipidaemia. The frequency of the L162V polymorphism in the PPARalpha gene was determined in 370 morbidly obese patients who underwent gastric banding surgery, 154 patients attending a type 2 DM clinic, 188 patients attending a lipid clinic and 199 healthy blood donors. The overall frequency of the V allele of the L162V polymorphism was 0.06. There were no significant differences in the allele frequency between patients with morbid obesity, hyperlipidaemia, type 2 DM and healthy controls, suggesting that it does not play a major role in the development of these conditions. The polymorphism was associated with a lower body mass index (BMI) in two independently recruited groups of patients with type 2 DM. There was no effect of the polymorphism on subjects without type 2 DM. Thus a polymorphism in PPARalpha protects type 2 DM patients from the overweight which is frequently associated with their condition.

Adult↗

Association between the P12A and c1431t polymorphisms in the peroxisome proliferator activated receptor gamma (PPAR gamma) gene and type 2 diabetes.

Variation in the peroxisome proliferator-activated receptor gamma (PPAR gamma) gene may play a role in the development of type 2 diabetes mellitus. Therefore we investigated the association between the P12A and c1431t polymorphisms in the PPAR gamma gene and type 2 diabetes. The incidence of the P12A polymorphism was determined by PCR-RFLP and the c1431t by single-strand conformation polymorphism analysis in 219 patients with, and 429 without type 2 diabetes. The frequency of the A allele of P12A polymorphism was 0.16 and the t allele of c1431t polymorphism, 0.13 in patients with type 2 diabetes, and 0.13 and 0.12 respectively in subjects without diabetes 3.2% of patients with and 1.4% without type 2 diabetes were A12A. Since the polymorphisms are not linked the association of the 9 possible genotypes with type 2 diabetes was determined. All patients with genotype A12A/c1431c had type 2 diabetes (n = 3, p = 0.038). There was no association between A12A/t1431t and diabetes. DNA sequencing revealed no additional mutations in the coding region of the PPAR gamma gene in genotypes A12A/c1431c or A12A/t1431t. The associations found between polymorphisms in the PPAR gamma gene and type 2 diabetes suggest that either the A12 isofrom is functional leading to a predisposition to type 2 diabetes in homozygotes or that there is a third, unknown mutation linked to the A12/c1431 haplotype which is responsible.

Adult↗

Annexin VI stimulates endocytosis and is involved in the trafficking of low density lipoprotein to the prelysosomal compartment.

Annexins are calcium-binding proteins with a wide distribution in most polarized and nonpolarized cells that participate in a variety of membrane-membrane interactions. At the cell surface, annexin VI is thought to remodel the spectrin cytoskeleton to facilitate budding of coated pits. However, annexin VI is also found in late endocytic compartments in a number of cell types, indicating an additional important role at later stages of the endocytic pathway. Therefore overexpression of annexin VI in Chinese hamster ovary cells was used to investigate its possible role in endocytosis and intracellular trafficking of low density lipoprotein (LDL) and transferrin. While overexpression of annexin VI alone did not alter endocytosis and degradation of LDL, coexpression of annexin VI and LDL receptor resulted in an increase in LDL uptake with a concomitant increase of its degradation. Whereas annexin VI showed a wide intracellular distribution in resting Chinese hamster ovary cells, it was mainly found in the endocytic compartment and remained associated with LDL-containing vesicles even at later stages of the endocytic pathway. Thus, data presented in this study suggest that after stimulating endocytosis at the cell surface, annexin VI remains bound to endocytic vesicles to regulate entry of ligands into the prelysosomal compartment.

Animals↗

Variation in the gene for human peroxisome proliferator activated receptor gamma (PPARgamma) does not play a major role in the development of morbid obesity.

OBJECTIVE: To determine the extent of variation in the gene for peroxisome proliferator activated receptor gamma (PPARgamma) in patients with morbid obesity. SUBJECTS: Two hundred morbidly obese patients who underwent gastric banding surgery and 192 healthy blood donors. Diabetics were excluded. EXPERIMENTAL: The frequency of the P115Q and P12A variants in the PPARgamma gene was determined. Single strand conformational polymorphism (SSCP) analysis was performed on all exons, exon/intron boundaries and part of the promoter of the PPARgamma gene on a sub-group of 67 morbid obese patients. RESULTS: None of the morbid patients or the blood donors were carriers of the P115Q mutation. The frequency of the P12A polymorphism did not differ significantly between morbid obese patients and controls and there was no statistically significant association between P12A and BMI. Male blood donors who were A12A homozygotes had statistically significant higher serum leptin concentrations (P = 0.001). Mutation screening revealed that one patient had a T -->G transversion at -208 in the promoter of PPARgamma-2, two had silent mutations, one a T-->C transition in the third base of codon 144 and the other a C-->T transition in codon 297. The fourth patient had a CGC-->TGC transition in codon 316 resulting in the replacement of an arginine with a cysteine. This mutation was not found in any other morbidly obese patient. CONCLUSION: Variation in the PPARgamma gene is unlikely to play a major role in the development of morbid obesity.

Adult↗

Frequency of and interaction between polymorphisms in the beta3-adrenergic receptor and in uncoupling proteins 1 and 2 and obesity in Germans.

OBJECTIVE: To determine the role of polymorphisms in the genes for beta3-adrenergic receptor (beta3-AR) and in uncoupling proteins 1 and 2 (UCP-1, UCP-2) in obesity. DESIGN: Association study with three polymorphisms and obesity. SUBJECTS: Two hundred and thirty-six morbidly obese patients who underwent gastric banding surgery, 381 patients from the medical clinic and 198 healthy blood donors. MEASUREMENTS: The frequencies of the W64R in beta3-AR, the 3826A-->G in UCP-1 and the 45bp insertion in the 3 untranslated region of exon 8 in UCP-2 polymorphisms were determined. RESULTS: There were no significant differences in the frequencies of the beta3-AR and UCP-1 polymorphisms between obese (body mass index, BMI > 30 kg/m2) and lean subjects. Lean, but not obese, carriers of the R allele of beta3-AR had a significantly higher BMI. The mean age of obese subjects (excluding diabetics) who were carriers of the G allele of the UCP-1 polymorphism, 36y, was significantly younger than wild-type, 40y (P= 0.007). This effect was not seen in lean subjects. The effect of the G allele on the mean age of obese subjects was more apparent in subjects who were also carriers of the R allele of the beta3-AR polymorphism. The frequency of the ins allele of UCP-2 was significantly higher in obese subjects, 0.31, than in lean, 0.24 (P= 0.002) and carriers of the ins allele had a significantly higher BMI, 38 vs 35 (P= 0.005). There was no association between any of the polymorphisms and type II diabetes. CONCLUSION: In a German population, there was no association between the W64R in beta3-AR or the 3826A-->G in UCP-1 polymorphisms and obesity. However, they act synergistically to accelerate the development of obesity. The 45bp insertion in the 3 untranslated region of exon 8 in UCP-2 polymorphism is associated with obesity.

Adult↗

Lack of association between a human beta-2 adrenoceptor gene polymorphism (gln27glu) and morbid obesity.

OBJECTIVE: To determine the frequency of the gln27glu polymorphism in the beta-2 adrenoceptor gene in patients with morbid obesity. SUBJECTS: 243 patients with morbid obesity (mean body mass index 51. 6) and 199 healthy blood donors. RESULTS: The same frequency, 0.42, of the glu allele was observed in both groups. Neither the incidence in obese women (0.41, n=197) compared to control women (0.43, n=61), nor that in obese men (0.44, n=46) compared to control men (0.41, n=138) was significantly different. The difference in frequency between obese men and women, 0.44 vs 0.41 was not significant (P=0. 68). Genotype information from the families of 18 of the obese patients showed no association between the glu27 allele and BMI. CONCLUSIONS: We find no evidence for a role of the glu27 variant in the beta-2 adrenoceptor gene in the development of morbid obesity.

Alleles↗

Compound heterozygosity for a new (S259G) and a previously described (G188E) mutation in lipoprotein lipase (LpL) as a cause of chylomicronemia. Mutations in brief no. 183. Online.

Familial chylomicronemia is an autosomal recessive disease characterised by fasting triglyceridemia and an absence of lipoprotein lipase (LpL) activity in post-heparin plasma. The disease is a result of mutation in either the lipoprotein lipase (Lpl) gene or in the apoCII gene which codes for an essential co-factor. To date, over 80 mutations in the LpL gene have been reported. The proband, a 30 month old female, presented with fasting triglycerides of 3192 mg/dl, and no detectable LpL mass or activity in post-heparin plasma. Sequencing of all of the exons and exon/intron boundaries of the LpL gene showed that she was a compound heterozygote with G-A transitions in codon 188 (G188E:GGG to GAG) generating an avall restriction site and in codon 259 (S259G:AGT to GGT) generating a bssKI site. Restriction digests confirmed the mutations and determined the incidence within the family. The father (55%LPL activity), paternal aunt (82%) and paternal grandmother (29%) were all heterozygous for the S259G mutation whilst her sister (55%), mother (73%) and maternal grandfather (45%) were heterozygous for the G188E mutation. The maternal grandmother (114%) was unaffected.

Female↗

Subendocardial infarction produces epicardial parasympathetic denervation in canine left ventricle.

Forty dogs underwent anterior descending coronary artery dissection with most having occlusion that was either maintained or reperfused. Study was performed 1-4 days later. Multiple electrodes placed in normal and ischemic zones were used to determine the depth of the epicardial rim overlying a subendocardial infarction. This was done by comparing voltage differential with respect to time (dV/dt) measurements of sequential bipolar electrograms along each needle. By this means, test sites with a rim were documented, and depths of epicardial biopsies for choline acetyltransferase were chosen. Epicardial effective refractory period (ERP) responses to vagal nerve stimulation were measured. In sham-operated controls, vagal stimulation prolonged ERP, and choline acetyltransferase activity was equivalent in all sites. In contrast, dogs with all durations of coronary occlusion and various thicknesses of subendocardial infarction had no significant prolongation of ERP limited to rim sites overlying the infarct during vagal nerve stimulation. Corresponding choline acetyltransferase activity was decreased in rim sites compared with remote areas. In addition, dogs given norepinephrine or physostigmine (to potentiate parasympathetic responses) did not demonstrate significant ERP prolongation with vagal stimulation. Infusion of acetylcholine into the distal ligated coronary artery produced dose-dependent prolongation of ERP in sites overlying the infarct. These data taken together support the hypothesis that subendocardial infarction, regardless of its homogeneity or thickness, produces parasympathetic denervation of the overlying epicardial rim.

Animals↗

Identical twins with hereditary hemorrhagic telangiectasia concordant for cerebrovascular arteriovenous malformations.

Central nervous system arteriovenous malformations are uncommon in hereditary hemorrhagic telangiectasia. Identical twins are described with hereditary hemorrhagic telangiectasia and concordance for central nervous system arteriovenous malformations identified by angiography. One twin had a central nervous system hemorrhage in the seventh month of pregnancy and also had a pulmonary arteriovenous malformation. The other was asymptomatic. A previously reported association between HLA type A2 BW17 and hereditary hemorrhagic telangiectasia was not confirmed. Two recombinations were identified between the loci for HLA and hereditary hemorrhagic telangiectasia. The loci for HLA and hereditary hemorrhagic telangiectasia are not closely linked. Stroke in a young person should prompt an inspection for manifestations of hereditary hemorrhagic telangiectasia.

Adult↗