Biomedical subjects

B Müller

Publications and source records attributed to B Müller.

At least 127 records · Page 7Linked to original sources

PubMed2000

Long-term survival of glioblastoma multiforme: importance of histopathological reevaluation.

The overall prognosis for patients with glioblastoma multiforme is extremely poor. However, a small proportion of patients enjoy prolonged survival. This study investigated retrospectively the extent to which erroneous histopathological classification may contribute to long-term survival of patients initially diagnosed with "glioblastoma multiforme." We compared two age- and gender-matched patient groups with different postoperative time to tumor progression (TTP), defined as "short-term" for TTP of less than 6 months (n = 54), and "long-term" for TTP of more than 12 months (n = 52). Histological specimens of the corresponding tumors, all primarily diagnosed as glioblastoma multiforme, were reevaluated according to the current World Health Organization (WHO) classification of central nervous system tumors, with the investigators being blinded to clinical outcome. Among the tumors from short-term TTP patients, one tumor (2%) was reclassified as anaplastic oligoastrocytoma (WHO grade III) while the remaining 53 were confirmed as glioblastoma multiforme. In contrast, 13 tumors (25%) from the long-term TTP patients were reclassified, mostly as anaplastic oligodendroglioma (WHO grade III; n = 7) or anaplastic oligoastrocytoma (WHO grade III, n = 2), respectively. In addition, three were reclassified as anaplastic astrocytoma (WHO grade III), and one was identified as anaplastic pilocytic astrocytoma (WHO grade III). Our data indicate that a sizable proportion of glioblastoma patients with long-term survival actually carry malignant gliomas with oligodendroglial features. The correct histopathological recognition of these tumors has not only prognostic but also therapeutic implications, since oligodendroglial tumors are more likely to respond favorably to chemotherapy.

Adult↗

PubMed2000

Proliferation and number of Clara cell 10-kDa protein (CC10)-reactive epithelial cells and basal cells in normal, hyperplastic and metaplastic bronchial mucosa.

Clara cell 10-kDa protein (CC10) is an inhibitor of phospholipase A2 and binds to phosphatidylinositol. It may therefore interfere with intracellular signal transduction. Bronchial CC10-reactive cells have been described by several authors. In contrast to the bronchiolar CC10-containing Clara cell, which is a progenitor cell of terminally differentiated airway epithelium, the role of bronchial CC10-reactive cells remains to be elucidated. We assessed the number of bronchial CC10-reactive cells in relation to cytokeratin (CK) expression and proliferative activity in normal, hyperplastic and squamous metaplastic epithelium. Sixty-five human bronchial mucosal specimens were investigated immunohistochemically for CK expression (CK7, CK13 and CK5/6), proliferative activity (MIB-1) and number of CC10-reactive epithelia. The proliferation fraction of CC10-reactive cells was assessed with double staining for MIB-1 and CC10. The proliferation index of the epithelium differed significantly between normal, hyperplastic and metaplastic epithelium. The number of CC10-reactive cells was inversely related to the epithelial proliferation. Bronchial CC10-reactive cells showed no proliferative activity as assessed using immunohistochemical double staining for CC10 and MIB-1. In contrast to normal and hyperplastic epithelium, squamous metaplasia disclosed CK5/6 in all epithelial layers, a loss of CK7 and a gain of CK13. We conclude that CC10-reactive cells have no progenitor role in the bronchial mucosa. However, because the proliferative activity is inversely related to the number of CC10-reactive cells, the CC10 protein may play a role in the regulation of epithelial repair. Squamous metaplasia most likely originates from basal cells.

Adult↗

PubMed2000

CD14, new aspects of ligand and signal diversity.

The glycosyl-phosphatidylinositol-linked glycoprotein CD14 is expressed in myeloid cells and serum. It binds Gram-negative and -positive bacterial cell wall components and endogenous phospholipids. Toll-like receptors, NF-kappaB and MAP kinases participate in CD14 signaling of inflammation. Alterations of CD14 in inflammatory diseases support a pathogenic role for this microbial receptor.

Animals↗

PubMed2000

Increased expression of human herpesvirus 7 in lymphoid organs of AIDS patients.

BACKGROUND: Human herpesvirus 7 (HHV-7) interferes reciprocally with the human immunodeficiency virus (HIV) in CD4 T lymphocytes, as infection with HIV results in a down modulation of the CD4 molecule and inhibition of replication of HHV-7, and vice versa. Correlations between HHV-7 and HIV at the organ level have not been studied in detail. OBJECTIVE: To study the presence and cellular distribution of HHV-7 in lymphoid organs, i.e. lymph nodes (LNs) and spleen in AIDS patients and HIV-seronegative individuals. STUDY DESIGN: Cross-sectional study. The detection of HHV-7 specific antigen pp85, the 85 kDa encoded tegument phosphoprotein by U14 gene, was performed by immunohistochemistry (IHC) with a well characterized monoclonal antibody (mAb 5E1) to pp85. Nested polymerase chain reaction (PCR) was applied to detect HHV-7 specific DNA sequences. RESULTS: Cells infected with HHV-7 were detected in five of seven LNs from AIDS patients and in one of five LNs from HIV-seronegative patients. The infected cells were mainly macrophages. In samples from HIV-seropositive patients, a significantly higher number of HHV-7 infected cells could be observed than in specimens from HIV-seronegative patients. Neither the antigen nor DNA sequences of HHV-7 could be detected in spleen tissue from HIV-seronegative and AIDS patients. CONCLUSIONS: The data indicate that HHV-7 undergoes a higher extent of reactivation from latency and/or of replication under immunosuppression due to HIV-infection, similar to the other beta-herpesviruses HHV-6 and human cytomegalovirus (HCMV). The data further suggest that LNs, but not the spleen, may be a site of latency and consequently of reactivation of HHV-7 in AIDS patients.

Acquired Immunodeficiency Syndrome↗

PubMed2000

Specificities of Caenorhabditis elegans and human hairpin binding proteins for the first nucleotide in the histone mRNA hairpin loop.

The 3' ends of animal replication-dependent histone mRNAs are formed by endonucleolytic cleavage of the primary transcripts downstream of a highly conserved RNA hairpin. The hairpin-binding protein (HBP) binds to this RNA element and is involved in histone RNA 3' processing. A minimal RNA-binding domain (RBD) of approximately 73 amino acids that has no similarity with other known RNA-binding motifs was identified in human HBP [Wang Z-F et al., Genes & Dev, 1996, 10:3028-3040]. The primary sequence identity between human and Caenorhabditis elegans RBDs is 55% compared to 38% for the full-length proteins. We analyzed whether differences between C. elegans and human HBP and hairpins are reflected in the specificity of RNA binding. The C. elegans HBP and its RBD recognize only their cognate RNA hairpins, whereas the human HBP or RBD can bind both the mammalian and the C. elegans hairpins. This selectivity of C. elegans HBP is mostly mediated by the first nucleotide in the loop, which is C in C. elegans and U in all other metazoans. By converting amino acids in the human RBD to the corresponding C. elegans residues at places where the latter deviates from the consensus, we could identify two amino acid segments that contribute to selectivity for the first nucleotide of the hairpin loop.

Amino Acid Sequence↗

PubMed2000

[Personality disorders and psychiatric morbidity in adolescent anorexia nervosa. Results of a prospective 10 year catamnesis].

The aim of the current prospective study was to examine at regular intervals the course of the eating disorder symptoms and the psychiatric (co-) morbidity including personality disorders among juvenile patients who fulfilled the DSM-III-R criteria for anorexia nervosa. Ten years after release from hospital all 39 patients (100%), as well as a control group parallelized for age, gender and occupational status were personally followed-up. Symptoms of eating disorders were documented by means of the Standardized Interview for Anorexia and Bulimia nervosa (SIAB, Fichter et al., 1991), the Composite International Diagnostic Interview (WHO, 1990) was applied to diagnose psychiatric (co-) morbidity, and the Structured Clinical Interview (SKID-II, Spitzer et al., 1993) to assess personality disorders. Compared to the control group, at the time of follow-up a significantly greater number of patients were suffering from a psychiatric disorder, primarily an anxiety disorder, an affective disorder or from drug, respectively alcohol abuse. Personality disorders, chiefly anxious-avoidant types on the DSM-III-R were diagnosed among almost one-fourth of the patients. Our findings indicate that anorexia nervosa is not a developmental disorder limited to puberty but a disorder associated both cross-sectionally as well as longitudinally with other psychiatric disorders.

Adult↗

PubMed2000

Schnurri mediates Dpp-dependent repression of brinker transcription.

Signalling by Decapentaplegic (Dpp), a member of the TGFbeta superfamily of signalling molecules, controls many aspects of Drosophila development by activating and repressing target genes. Several essential components of the Dpp signalling pathway have been identified, including the Dpp receptors Punt and Thick veins (Tkv) as well as the cytoplasmic mediators Mad and Medea. For target genes to be activated, Dpp signalling must suppress transcription of a repressor encoded by the brinker (brk) gene. Here we show that Schnurri (Shn), a large zinc-finger protein, is essential for Dpp-mediated repression of brk transcription; in contrast, Shn is not required for target-gene activation. Thus, the Dpp signalling pathway bifurcates, downstream of the signal-mediating SMAD proteins, into a Shn-dependent pathway leading to brk repression and a Shn-independent pathway leading to gene activation. The existence of several Shn-like proteins in vertebrates and the observation that Brk functions in BMP signalling in Xenopus indicates that a similar regulatory cascade may be conserved in higher organisms.

Animals↗

PubMed2000

Disordered calcium homeostasis of sepsis: association with calcitonin precursors.

BACKGROUND: Hypocalcemia and increased serum levels of calcitonin precursors are common in critically ill patients, especially in those with sepsis. We investigated calcium homeostasis in such patients. PATIENTS AND METHODS: Serum concentrations of total and ionized calcium and known factors influencing or reflecting calcium homeostasis were measured in 101 consecutive patients of a medical intensive care unit. Calcitonin precursor levels were determined using a highly sensitive radioimmunoassay. RESULTS: Critical illness per se was associated with decreased serum total and ionized calcium levels, which correlated with the severity of the underlying disease as measured by the APACHE II score. In addition, total and ionized hypocalcemia was more pronounced with increasing severity of infection (P < 0.02), and occurred in parallel with a marked increase of calcitonin precursors (P < 0.001). Mature calcitonin levels, however, remained normal. Changes of serum ionized calcium concentrations from admission to discharge correlated significantly with changes in the serum calcitonin precursor concentration (r2 = - 0.14, P < 0.001). Circulating vitamin D levels, parathyroid hormone levels and other markers reflecting calcium homeostasis did not correlate with the severity of infection. CONCLUSIONS: In critically ill patients with sepsis, markedly elevated circulating calcitonin precursors might play a role in the development of the pronounced hypocalcemia. The specific calcitonin precursor(s) responsible for this effect and the pathophysiological mechanism remain to be elucidated.

Adult↗

PubMed2000

alpha-tocopherol improves impaired physiology of rat type II pneumocytes isolated from experimentally injured lungs.

BACKGROUND: Oxidant stress delivered by nitrogen dioxide (NO2) inhalation impairs the function of extracellular surfactant as well as surfactant phospholipid metabolism in type II pneumocytes. Because protection against oxidant stress is important to normal lung function, the lung contains a variety of antioxidants, including vitamin E. Whether administration of this antioxidant during NO2 inhalation attenuates NO2-induced alterations in phospholipid metabolism in type II pneumocytes has not been studied. METHODS: We exposed rats to identical NO2 body doses (720 p.p.m. x h) using continuous, intermittent, or repetitive protocols. During exposure periods, the animals received daily intramuscular injections of vitamin E (25 mg kg-1). We isolated type II pneumocytes from NO2-exposed rats and evaluated them for cell yield and viability, as well as for synthesis and secretion of phosphatidylcholine (PC) as measures of surfactant metabolism. RESULTS: The yield of type II pneumocytes was significantly elevated from animals that had been exposed continuously to NO2 whereas in intermittently and repeatedly exposed rats, cell yield was similar to yield from control animals. Viability of the isolated cells was similar in controls and all NO2 exposure protocols. Vitamin E treatment of the NO2-exposed rats neither changed cell yield nor cell viability. Phospholipid de novo synthesis, as estimated by choline incorporation into PC, was increased most after continuous NO2 inhalation whereas in the other conditions there was only a slight increase. Vitamin E administration further increased phospholipid synthesis; this difference reached statistical significance only in the case of intermittent NO2 exposure. Secretion of phosphatidylcholine from type II cells was only reduced after continuous NO2 inhalation and administration of the antioxidant reduced the impairment. CONCLUSION: Because vitamin E appears to preserve the ability of type II pneumocytes isolated from NO2-exposed rats to synthesize and secrete surfactant lipid, we conclude that administration of vitamin E may mitigate NO2-induced lung injury.

Administration, Inhalation↗

PubMed2000

An acidic microenvironment impairs the generation of non-major histocompatibility complex-restricted killer cells.

The microenvironment within solid tumours has often been shown to exhibit an acidic local pH. In recent studies we could demonstrate that an acidic extracellular pH (pHe) inhibits the non-major histocompatibility complex (MHC) -restricted cytotoxicity of immunocompetent effector cells. However, within tumours the activation of cytotoxic cells may already be impaired by low pHe. Therefore, we investigated the influence of acidic conditions on the generation of active killer cells. The cytotoxic activity of natural killer (NK) as well as lymphokine-activated killer (LAK) cells against K562, Daudi and Raji cells was analysed after an activation period of 3 days at pHe 7.2-6.5. A minor reduction of pHe from 7.2 to 7.0 during the culture period resulted in a strong inhibition of the natural cytotoxicity of NK cells. Furthermore, acidic pHe below 7.2 prevented the generation of activated LAK cells by interleukin-2 (IL-2). The cytotoxic capacity could not be reconstituted if cells cultured at a pHe of 6.5 were returned to physiological pH for another 24 hr. Analysis of the cellular subtypes within the various cultures did not reveal differences regarding the frequencies of NK cells, CD8+ T cells, or CD4+ T cells. However, an acidic pHe clearly inhibited the activation-induced increase of relevant adhesion molecules. The production of cytokines which are involved in the regulation of the cytotoxic process (tumour necrosis factor-alpha, interferon-gamma, IL-10, IL-12 and transforming growth factor-beta1) was also affected by pHe, as their release was strongly inhibited at pHe 7.0. Furthermore, we observed a considerable decrease in the metabolic activity of effector cells at acidic pHe. In summary, our findings suggest that an acidic microenvironment impairs the induction of an anti-tumoral immune response within solid tumours.

CD4-Positive T-Lymphocytes↗

PubMed2000

[Acute retinal necrosis syndrome: analysis, therapy and long-term follow up of 14 eyes].

PURPOSE: Acute retinal necrosis syndrome (ARN) might be complicated by retinal detachment, vasculopathy and optic neuropathy and has a poor prognosis despite intensive medical and surgical therapy. PATIENTS AND METHODS: A series of 10 consecutive patients (14 eyes) with ARN were followed for 36 months (average of 20 months +/- 10). We present the results of the clinical evaluation for diagnostic and therapeutic modalities. RESULTS: Viral etiology was confirmed in 9 of 10 aqueous-humor samples. Intraocular antibody synthesis against Varicella-Zoster Virus was found in 7, against Herpes-Simplex Virus in 5 and against Cytomegalovirus in 2 samples. Three eyes had a mild clinical course with a visual acuity of 0.6 or better. Vitrectomy and silicone-oil tamponade preserved visual acuity from 0.3 to 0.1. ARN lead to blindness in 5 eyes due to vasculopathy, optic neuropathy or retinal detachment. An arterial branch occlusion was successfully overcome with i.v. heparin treatment in one patient. CONCLUSION: Aqueous-humor analysis supports clinical diagnosis. Early vitrectomy and silicone oil tamponade stabilizes retinal structure and preserves visual acuity. Occlusive vasculopathy and optic neuropathy are the main causes leading to blindness.

Acyclovir↗

PubMed2000

Calcitonin precursors are reliable markers of sepsis in a medical intensive care unit.

OBJECTIVE: The diagnosis of infection in critically ill patients is challenging because traditional markers of infection are often misleading. For example, serum concentrations of calcitonin precursors are increased in patients with infections. However, their predictive accuracy for the diagnosis of sepsis in unselected patients in a medical intensive care unit (ICU) is unknown. Therefore, we compared the usefulness of serum concentrations of calcitonin precursors, C-reactive protein, interleukin-6, and lactate for the diagnosis of sepsis in consecutive patients suffering from a broad range of diseases with an anticipated stay of > or =24 hrs in a medical ICU. DESIGN: Prospective cohort study. SETTING: Medical intensive care unit in a university medical center. PATIENTS: 101 consecutive critically ill patients. INTERVENTION: None. MEASUREMENTS AND MAIN RESULTS: Blood samples were collected at various time points during the course of the disease. Systemic inflammatory response syndrome, sepsis, severe sepsis, and septic shock were diagnosed according to standardized criteria, and patients were reclassified daily without prior knowledge of the serum concentrations of calcitonin precursors or interleukin-6. At admission, 99% of the patients had systemic inflammatory response syndrome, 53% had sepsis, and 5% developed sepsis during their stay in the ICU. Calcitonin precursors, C-reactive protein, interleukin-6, and lactate levels increased with the severity of infection (p < .01, one-way analysis of variance). In a receiver operating characteristic curve analysis, calcitonin precursors were found to be the most reliable laboratory variable for the diagnosis of sepsis as compared with C-reactive protein, interleukin-6, and lactate (p < .01, for each comparison). Calcitonin precursor concentrations of >1 ng/mL had sensitivity of 89% and specificity of 94% for the diagnosis of sepsis. High serum concentrations of calcitonin precursors were associated with poor prognosis (p = .01). CONCLUSIONS: In a medical ICU, serum calcitonin precursor concentrations are more sensitive and are specific markers of sepsis as compared with serum C-reactive protein, interleukin-6, and lactate levels.

Adult↗

PubMed2000

Bacterial phosphating of mild (unalloyed) steel.

Mild (unalloyed) steel electrodes were incubated in phosphate-buffered cultures of aerobic, biofilm-forming Rhodococcus sp. strain C125 and Pseudomonas putida mt2. A resulting surface reaction leading to the formation of a corrosion-inhibiting vivianite layer was accompanied by a characteristic electrochemical potential (E) curve. First, E increased slightly due to the interaction of phosphate with the iron oxides covering the steel surface. Subsequently, E decreased rapidly and after 1 day reached -510 mV, the potential of free iron, indicating the removal of the iron oxides. At this point, only scattered patches of bacteria covered the surface. A surface reaction, in which iron was released and vivianite precipitated, started. E remained at -510 mV for about 2 days, during which the vivianite layer grew steadily. Thereafter, E increased markedly to the initial value, and the release of iron stopped. Changes in E and formation of vivianite were results of bacterial activity, with oxygen consumption by the biofilm being the driving force. These findings indicate that biofilms may protect steel surfaces and might be used as an alternative method to combat corrosion.

Biofilms↗

PubMed2000

Human immunodeficiency virus type 1 Vpr protein is incorporated into the virion in significantly smaller amounts than gag and is phosphorylated in infected cells.

Viral protein R (Vpr) of human immunodeficiency virus type 1 (HIV-1) is a small accessory protein involved in the nuclear import of viral DNA and the growth arrest of host cells. Several studies have demonstrated that a significant amount of Vpr is incorporated into the virus particle via interaction with the p6 domain of Gag, and it is generally assumed that Vpr is packaged in equimolar ratio to Gag. We have quantitated the relative amount of Vpr in purified virions following [(35)S]cysteine labeling of infected MT-4 cells, as well as by quantitative immunoblotting and found that Vpr is present in a molar ratio of approximately 1:7 compared to capsid. Analysis of isolated core particles showed that Vpr is associated with the mature viral core, despite quantitative loss of p6 from core preparations. Metabolic labeling of infected cells with ortho[(32)P]phosphate revealed that a small fraction of Vpr is phosphorylated in virions and infected cells.

Capsid↗

PubMed2000

The effect of repeated ozone exposures on inflammatory markers in bronchoalveolar lavage fluid and mucosal biopsies.

The aim of this study was to investigate the cellular and biochemical events associated with repeated exposures to ozone. Twenty-three healthy subjects underwent single exposures to 200 ppb ozone and to filtered air (FA), as well as repeated exposures to 200 ppb ozone on 4 consecutive days, each for 4 h of intermittent exercise. Bronchoalveolar lavage was performed and mucosal biopsies were taken 20 h after the single or the last of the repeated exposures. As compared with FA, the single exposure to ozone caused a decrease in FEV(1), an increase in the percentages of neutrophils and lymphocytes, the concentrations of total protein, IL-6, IL-8, reduced glutathione, urate, and ortho-tyrosine in BAL fluid (BALF), but no changes in the cellular composition of biopsy. After the repeated exposure, the effect on lung function was abolished and differential cell counts in BALF were not significantly different from those after FA. However, the concentrations of total protein, IL-6, IL-8, reduced glutathione, and ortho-tyrosine were still increased. IL-10 could only be detected in BALF after repeated ozone exposures. Furthermore, macroscopic scores for bronchitis, erythema, and hypervulnerability of airway mucosa were increased, as well as numbers of neutrophils in bronchial mucosal biopsies. Our data demonstrate that airway inflammation persists after repeated ozone exposure, despite attenuation of some inflammatory markers in BALF and adaptation of lung function.

Adult↗

PubMed2000

Differential genetic alterations in von Hippel-Lindau syndrome-associated and sporadic pheochromocytomas.

Pheochromocytomas arise sporadically and as a component tumor of the inherited cancer syndromes von Hippel-Lindau disease (VHL), multiple endocrine neoplasia type 2 (MEN 2), and type 1 neurofibromatosis. Germline mutations of the VHL tumor suppressor gene (VHL) are responsible for VHL, and germline RET protooncogene mutations are associated with MEN 2. The present study was conducted to examine a large series of 36 VHL-related pheochromocytomas for somatic VHL and RET gene alterations and loss of heterozygosity (LOH) of markers on chromosome arms 1p, 3p, and 22q. For comparison, the same analyses were performed in 17 sporadic pheochromocytomas. We found no somatic intragenic mutations within VHL and RET in any VHL or sporadic pheochromocytoma, and no pheochromocytoma demonstrated upstream VHL gene hypermethylation. Of interest, we found significantly different LOH frequencies at 3 loci between sporadic and VHL tumors; the more than 91% LOH of markers on 3p and the relatively low frequencies of LOH at 1p and 22q (15% and 21%, respectively) in VHL pheochromocytomas argue for the importance of VHL gene dysregulation and dysfunction in the pathogenesis of almost all VHL pheochromocytomas. In contrast, the relatively low frequency of 3p LOH (24%; P: << 0.0001) and the lack of intragenic VHL alterations compared with the high frequency of 1p LOH (71%; P: = 0.0003) and the moderate frequency of 22q LOH (53%) in sporadic pheochromocytomas argue for genes other than VHL, especially on 1p, that are significant for sporadic tumorigenesis and suggest that the genetic pathways involved in sporadic vs. VHL pheochromocytoma genesis are distinct.

Adrenal Gland Neoplasms↗

PubMed2000

The repressor and activator forms of Cubitus interruptus control Hedgehog target genes through common generic gli-binding sites.

The Drosophila Gli homolog Cubitus interruptus (Ci) controls the transcription of Hedgehog (Hh) target genes. A repressor form of Ci arises in the absence of Hh signalling by proteolytic cleavage of intact Ci, whereas an activator form of Ci is generated in response to the Hh signal. These different activities of Ci regulate overlapping but distinct subsets of Hh target genes. To investigate the mechanisms by which the two activities of Ci exert their opposite transcriptional effect, we dissect here the imaginal disc enhancer of the dpp gene, which responds to both activities of Ci. Within a minimal disc enhancer, we identify the DNA sequences that are necessary and sufficient for the control by Ci, show that the same sequences respond to the activator and repressor forms of Ci, and demonstrate that their activities can be replaced by a single synthetic Gli-binding site. We further show that the enhancer sequences of patched, a gene responding only to the activator form of Ci, effectively integrate also the repressor activity of Ci if placed into a dpp context. These results provide in vivo evidence against the employment of distinct binding sites for the different forms of Ci and suggest that target genes responding to only one form must have acquired distant cis-regulatory elements for their selective behavior.

Animals↗

PubMed2000

The influence of avascularity on the mechanical properties of human bone-patellar-tendon-bone grafts.

Our aim was to analyse the effect of avascularity on the morphology and mechanical properties (tensile strength, viscoelasticity) of human bone-patellar-tendon-bone (BPTB) grafts in vitro. These were harvested at postmortem and stored submerged in denaturated human plasma at a constant pH, pO2, pCO2, temperature and humidity under sterile conditions. Mechanical testing was performed two and four weeks after removal of the graft. The mean ultimate strength was 1085.7 +/- 255.8 N (control), 1009.0 +/- 314.9 N (two weeks cultured) and 1076.8 +/- 414.8 N (four weeks cultured). There was no significant difference in linear stiffness or deformation to failure between the groups. There was a difference in viscoelasticity between the control group and the avascular grafts and the latter had significant lower peak load-to-load ratios after 15 minutes compared with the control group. After two and four weeks the graft contained viable fibroblasts. There was regular cellularity in the superficial layers and decreased cellularity in the midportion. The structure of the collagen including the crimp pattern appeared to be normal in polarised light. We conclude that avascularity does not significantly affect ultimate failure loads or stiffness of BPTB grafts. Slight changes in viscoelasticity were induced, but the significance of the increased stress relaxation is not fully understood.

Adult↗