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Biomedical subjects

Ardeshir Bayat

Publications and source records attributed to Ardeshir Bayat.

At least 19 recordsLinked to original sources
PubMed2006

Use of a non-contact 3D digitiser to measure the volume of keloid scars: a useful tool for scar assessment.

Keloid scars often fail to respond to treatment, so research into new therapeutic regimes is important. However, research is limited by a scarcity of reliable, objective scar assessment tools. The volume of a keloid scar should decrease with successful treatment. This study demonstrates the use of a non-contact 3D digitiser to measure digitally the volume of a keloid scar. The scanner was used to scan 62 keloid scars and one fine-line normal scar. The scan took approximately 9s to complete. The volume was measured using 3D reverse modelling software. A previously validated scar assessment scale was used to score the scars according to their physical parameters. A significant correlation was found between volume and the scar score (Pearson's r=0.627, p<0.001). Linear regression was also statistically significant (p<0.001, R(2)=0.44). Therefore it was possible to predict the scar score from the measured volume. This technique could allow monitoring of a patient on treatment, or comparison of treatments in a research setting. It overcomes previous problems with the measurement of scar volume as it is quantitatively objective and well-tolerated.

Adult↗
PubMed2006

Decreased expression of inhibitory SMAD6 and SMAD7 in keloid scarring.

Keloids are benign skin tumours occurring during wound healing in genetically predisposed patients. They are characterised by an abnormal deposition of extracellular matrix components, in particular collagen. There is evidence that transforming growth factor-beta (TGFbeta) is involved in keloid formation. SMAD proteins play a crucial role in TGFbeta signaling and in terminating the TGFbeta signal by a negative feedback loop through SMAD6 and 7. It is unclear how TGFbeta signaling is connected to the pathogenesis of keloids. Therefore, we investigated the expression of SMAD mRNA and proteins in keloids, in normal skin and in normal scars. Dermal fibroblasts were obtained from punch-biopsies of keloids, normal scars and normal skin. Cells were stimulated with TGFbeta1 and the expression of SMAD2, 3, 4, 6 and 7 mRNA was analysed by real time RT-PCR. Protein expression was determined by Western blot analysis. Our data demonstrate a decreased mRNA expression of the inhibitory SMAD6 and 7 in keloid fibroblasts as compared to normal scar (p<0.01) and normal skin fibroblasts (p<0.05). SMAD3 mRNA was found to be lower in keloids (p<0.01) and in normal scar fibroblasts (p<0.001) compared to normal skin fibroblasts. Our data showed for the first time a decreased expression of the inhibitory SMAD6 and SMAD7 in keloid fibroblasts. This could explain why TGFbeta signaling is not terminated in keloids leading to overexpression of extracellularmatrix in keloids. These data support a possible role of SMAD6 and 7 in the pathogenesis of keloids.

Blotting, Western↗
PubMed2006

The heritability of Dupuytren's disease: familial aggregation and its clinical significance.

PURPOSE: Dupuytren's disease (DD) is a benign, fibroproliferative disease affecting the hands. The familial occurrence of DD and its presence in identical twins suggests a genetic basis for the condition. Our aims in this study were (1) to provide evidence for familial aggregation of DD by estimating the sibling recurrence-risk ratio and (2) to link previously associated environmental risk factors with family history of DD. METHODS: Patients diagnosed with DD between the ages of 58 and 81 years (N = 92) were interviewed to assess potential risks and the severity of their conditions. A clinical history and examination were performed and we attempted to interview every family member either in person or through a postal questionnaire. RESULTS: The sibling recurrence-risk ratio (lambda(s)) equaled 2.9 and ranged from 2.6 to 3.3 based on the 95% confidence intervals for the population prevalence. This suggests a high genetic basis for the causation of DD. A lower age of onset and greater severity of DD were associated significantly with a positive family history of DD. Other factors showed no statistical significance with familial aggregation of DD. CONCLUSIONS: The familial clustering observed in DD likely is due to genetic influence rather than shared environment, as shown by the lack of association with exposure to environmental risk factors and family history. Understanding the genetic basis of DD is important for developing novel diagnostic, preventative, and therapeutic regimens in the future. TYPE OF STUDY/LEVEL OF EVIDENCE: Prognostic, Level II.

Adult↗
PubMed2006

Dupuytren's diathesis revisited: Evaluation of prognostic indicators for risk of disease recurrence.

PURPOSE: The term diathesis relates to certain features of Dupuytren's disease (DD) and dictates an aggressive course of disease. The initial description of DD diathesis included 4 factors: (1) ethnicity, (2) family history, (3) bilateral DD, and (4) ectopic lesions (DD outside the palm). The degree of diathesis is considered important in predicting recurrence and extension of DD after surgical management. Prognostic indicators of risks associated with surgery are important. We aimed to evaluate these 4 factors and known associated risk factors to formulate a statistical predictive value for DD diathesis. METHODS: Caucasian patients diagnosed with DD between the ages of 25 and 90 years (n = 322) from Northwest England were assessed for DD diathesis with a clinical history and examination. DD diathesis assessment was analyzed by calculating the odds ratios of developing recurrent DD using logistic regression. RESULTS: The observed recurrence rates in the presence of notable risk factors and corresponding odds ratios of recurrent DD were calculated. Of note, recurrent disease was observed in 121 (46%) males, 105 (47%) with bilateral DD, 68 (48%) with a family history of DD, 75 (47%) with age at onset younger than 50 years, 35 (52%) in those with ectopic lesions, and in 26 (63%) with Garrod's pads. CONCLUSIONS: The original DD diathesis factors have been evaluated and modified. The original factors of family history, bilateral DD, and ectopic lesions now include 2 additional factors: male gender and age at onset of younger than 50 years. Family history and ectopic disease have now been modified to specify family history with one or more affected siblings/parents and ectopic lesions in the knuckles (Garrod's pads) alone. The presence of all new DD diathesis factors in a patient increases the risk of recurrent DD by 71% compared with a baseline risk of 23% in those DD patients with none of the earlier-described factors. TYPE OF STUDY/LEVEL OF EVIDENCE: Prognostic II.

Adult↗
PubMed2006

A technique for accurate and safe injection of steroid in trigger digits using ultrasound guidance.

Steroid injections have long been the main stay of conservative treatment of trigger digits. This procedure gives variable results, which is dependent on a number of factors. The injection of the steroid in the right place improves the success rate and also prevents complications associated with the procedure. We describe a technique using ultrasound for accurate injection of steroid to maximise its beneficial effects in treatment of trigger digits.

Humans↗
PubMed2005

Studies of transforming growth factors beta 1-3 and their receptors I and II in fibroblast of keloids and hypertrophic scars.

Keloids are benign skin tumours occurring during wound healing in genetically predisposed patients. They are characterized by an abnormal deposition of extracellular matrix components, particularly collagen. There is uncertain evidence that transforming growth factor-beta (TGFss) is involved in keloid formation. Therefore we investigated the expression of TGFss1, 2 and 3 and their receptors in keloids, hypertrophic scars and normal skin. Dermal fibroblasts were obtained from punch biopsies of patients with keloids and hypertrophic scars and from normal skin of healthy individuals. Total RNA was isolated and the expression of TGFss1, 2 and 3 and of TGFss receptors I and II (TGFssRI and II) was analysed by real-time PCR using the Lightcycler technique. Our data demonstrate significantly lower TGFss2 mRNA expression in hypertrophic scar fibroblasts as compared with fibroblasts derived from keloids and normal skin (p<0.05). In contrast, TGFss3 mRNA expression was significantly lower in keloid fibroblasts in comparison with fibroblasts derived from hypertrophic scar and normal skin (p<0.01). TGFssRI mRNA expression was significantly decreased in hypertrophic scar fibroblasts (p<0.01) and TGFssRII mRNA expression was decreased in keloids compared with hypertrophic scar fibroblasts (p<0.001). The ratio of TGFssRI/TGFssRII expression was increased in keloids compared with hypertrophic scar and normal skin fibroblasts. As recently supposed, an increased TGFssRI/TGFssRII ratio could promote fibrosis. Therefore our data support a possible role of TGFssRI and TGFssRII in combination with a certain TGFss expression pattern as fibrosis-inducing factors in keloids.

Case-Control Studies↗
PubMed2005

Identification of a novel mitochondrial mutation in Dupuytren's disease using multiplex DHPLC.

Dupuytren's disease is a familial fibroproliferative disorder of late onset affecting the hands. It is extremely common in individuals of Northern European extraction. Genetic studies have yet to identify the genes involved in the formation of the disease. Mitochondria play a critical role in cell metabolism and apoptosis. It is known that defective mitochondria generate abnormally high levels of reactive oxygen species by means of electron leak and that antioxidant enzyme activities decrease with age in skin fibroblasts. Respiratory function of mitochondria is also impaired in aging human tissues. Oxidative stress and production of free radicals may be important factors in the pathogenesis of Dupuytren's disease. Mitochondrial genes are also included in the regulation of apoptosis. Diseased tissue contains large numbers of myo- fibroblasts, which disappear by apoptosis during normal wound healing. High numbers of mitochondria have been observed in fibroblasts derived from diseased tissue. In the light of this evidence, the mitochondrial genome represents a potential location for candidate susceptibility genes for this late-onset disorder. In this study, the authors investigated the presence of mutations within the mitochondrial genome in 40 subjects; 20 Caucasian Dupuytren's disease patients with a maternally transmitted inheritance pattern and 20 control subjects were matched for age, sex, and race using a multiplex denaturing high-performance liquid chromatography approach. A hitherto unknown heteroplasmic mutation located within the mitochondrial 16s rRNA region was evident in 90 percent of patients and absent from all control subjects (p < 0.001; chi2 = 16.1). This mutation may be important in the pathogenesis of Dupuytren's disease.

Adult↗
PubMed2004

Genetic susceptibility to keloid disease: transforming growth factor beta receptor gene polymorphisms are not associated with keloid disease.

Keloid disease (KD) is an abnormal form of scarring with a familial predisposition. Genetic studies have yet to identify the genes involved in KD. Transforming growth factor beta (TGF-beta) has multiple cellular activities including cellular proliferation, differentiation and extracellular matrix production. TGF-beta family members such as TGF-beta(1) and TGF-beta(2) are known to be involved in KD formation. However, we previously demonstrated a lack of association between common TGF-beta(1) and TGF-beta(2) polymorphisms and KD. Other studies have implicated TGF-beta receptors in KD pathogenesis. TGF-beta receptors were therefore selected as candidate-susceptibility genes for this condition. Single-nucleotide polymorphisms (SNPs) in TGF-beta receptors I, II and III (TGF-betaRI, TGF-betaRII and TGF-betaRIII) were identified and investigated for association with the risk of developing KD. A polymerase chain reaction-restriction fragment length polymorphism method was used for genotyping novel and known TGF-beta receptor polymorphisms. DNA samples from 92 KD cases and 181 controls were examined. There were no statistically significant differences in genotype or allele frequency distributions between cases and controls for the TGF-beta receptor SNPs. Therefore, these TGF-beta receptor polymorphisms are unlikely to be associated with keloid scarring. It is possible that other SNPs in other TGF-beta family members are associated with KD. To our knowledge, this is the first report of a case-control association study with KD and TGF-beta receptor gene polymorphisms.

Case-Control Studies↗
PubMed2003

Genetic susceptibility to keloid disease and hypertrophic scarring: transforming growth factor beta1 common polymorphisms and plasma levels.

Keloid disease and hypertrophic scars are dermal tumors that are often familial and typically occur in certain races. Their exact etiology is still unknown. Transforming growth factor beta1 (TGF-beta1) plays a central role in wound healing and fibrosis and has been implicated in the pathogenesis of keloid disease and hypertrophic scar. The aims of this study were to measure the plasma level of TGF-beta1 in patients compared with controls, and to investigate the association of five common single nucleotide polymorphisms in TGF-beta1 with the risk of keloid disease and hypertrophic scar formation. Platelet-poor plasma levels of TGF-beta1 in 60 patients (15 with hypertrophic scar and 45 with keloid disease) and 18 controls were measured using an enzyme-linked immunoabsorbent assay technique. A polymerase chain reaction-restriction fragment length polymorphism method was used for genotyping TGF-beta1 polymorphisms. DNA samples from 133 patients (101 with keloid disease and 32 with hypertrophic scar) and 200 controls were examined. All patients and controls were Caucasians of Northern European extraction. There was no statistically significant difference in TGF-beta1 plasma levels between patients with keloid disease and hypertrophic scar and controls. There was also no statistically significant difference in genotype or allele frequency distributions between patients and controls for codons 10, 25, and 263 and for -509 and -800 single nucleotide polymorphisms of the TGF-beta1 gene. These results suggest that TGF-beta1 plasma levels and common polymorphisms are not associated with a risk of keloid disease and hypertrophic scar formation. This lack of association may be significant in view of the importance attached to the role of TGF-beta1 in dermal scarring. To the authors' knowledge, this is the first report of a case-control association study in keloid disease and hypertrophic scars using any single nucleotide polymorphisms.

Adolescent↗
PubMed2003

Genetic susceptibility to dupuytren disease: association of Zf9 transcription factor gene.

Transforming growth factor beta 1 (TGF-beta 1) is a key fibrogenic cytokine that has been shown to stimulate fibroblast proliferation and extracellular matrix deposition and has been implicated in the pathogenesis of Dupuytren disease. Zf9 is a transcription factor that increases TGF-beta 1 expression in tissue. The authors previously demonstrated a lack of association between common TGF-beta 1 and TGF-beta 2 polymorphisms and Dupuytren disease. Therefore, Zf9 transcription factor represents an additional candidate susceptibility gene for investigating hereditary predisposition to Dupuytren disease. Dupuytren disease, or Dupuytren contracture, is a progressive and recurrent fibroproliferative disease of unknown etiology that affects the human hands. It is often a familial disorder affecting Northern European Caucasians. Genes implicated in the development of Dupuytren disease have not yet been found. Using a polymerase chain reaction-restriction fragment polymorphism method, the authors genotyped a novel single nucleotide polymorphism in the 3' untranslated region of the Zf9 gene. A case-control association study of 138 patients with Dupuytren disease versus 255 controls demonstrated a statistically significant difference in the genotype and allele frequencies between patients and controls for Zf9 gene polymorphism. Presence of the G allele versus the A allele is associated with an increased risk of developing Dupuytren disease (odds ratio, 1.9; 95 percent confidence interval, 1.2 to 2.9). The authors believe this to be the first report of a positive genetic association study in Dupuytren disease using single nucleotide polymorphisms.

Adult↗