de Quervain_s disease is a commonly encountered problem; its management is multimodal, and often, there is recurrence which is commonly associated with anatomical variation in the first dorsal compartment of the wrist. Our purpose was to find out the anatomical variation of the first dorsal compartment of the wrist in the general population to assess the anatomical basis of de Quervain_s disease and its recurrence. In this cadaveric study, 86 wrists in 46 patients were dissected to search out the first dorsal compartment of the wrist and its content tendons, presence of septa in the compartment, and insertion of the tendons. Supernumerary tendons in the first dorsal compartment were seen in 74.41 % of cases. The most commonly found tendon arrangement was two abductor pollicis longus (APL) and one extensor pollicis brevis (EPB). In all cases, there was a fixed insertion of APL to the base of the first metacarpal. Among other sites, the most common site of insertion of APL is the trapezium, which was 56.14 %. Variations of EPB with respect to number, site of insertion, thickness, and bilaterality were also found. The presence of septations was found in 37.20 % of dissected cadaveric wrists. We had found supernumerary tendons or slips in the first dorsal compartment very commonly. The presence of a septum was less frequently found. So, it may be concluded that there is immense anatomical variation present in the first dorsal compartment of the wrist, supernumerary tendons/tendon slips are commonly found, there is a variation of insertions present in the population, septum/aberrant compartment are also present, and bilateral variations are present in the population. These variations may be responsible for recurrence and unilateral affection in de Quervain_s disease. Keywords
Out of the three indices, APRI index with a NPV of 95% appeared to be a better model for excluding significant liver fibrosis while FIB-4 with a PPV of 61% showed fair correlation with significant fibrosis. Thus, these two non-invasive models for predicting of liver fibrosis, namely APRI and FIB-4, can be utilized in combination as screening tools in monitoring of CHB patients, especially in resource limiting settings.
Objective:Deltoid contracture is not uncommon in India. Contractures of deltoid often do not have definite etiology. We have critically analyzed the condition as regards the etiopathogenesis and its surgical results.Materials and Methods:Nineteen patients with deltoid contracture operated between June 1990 and September 2001 were enrolled for a unicentric retrospective study. The surgery was indicated in patients with abduction deformity of more than 30° at the shoulder. The etiology of deltoid contracture was idiopathic (n = 13) intramuscular injection in deltoid muscle (n = 5) and blunt trauma (n = 1). All were operated by distal release (incision near the insertion of the deltoid muscle). The average follow-up was of 9.5 years (range 6-17 years). They were evaluated based on parameters like pain, persistence of deformity, range of shoulder movements and strength of deltoid.Results:All patients recovered painless full range of shoulder motion except one. The correction of deformity was achieved in all patients and there was no loss of strength of deltoid compared to the opposite side. Histology of excised tissue showed features of chronic inflammation. The complications observed were hypertrophic scar (n = 1), painful terminal restriction of shoulder movements (n = 1) and prominent vertebral border of scapula (n = 1).Conclusion:Deltoid contracture has features of chronic inflammation, and the intramuscular deltoid injection is the most incriminating factor in its etiopathogenesis. The condition can be effectively managed surgically by distal release of the deltoid muscle combined with excision of the muscular fibrotic contracture band.
The mucin gene is up-regulated in diseases such as cystic fibrosis (CF) and asthma. To understand the mechanisms involved in transcriptional regulation of mucin gene expression we have characterized the region of the mucin gene up-stream of the transcriptional start site and analysed the cis-acting elements required for mucin promoter activity. We isolated clones from a dog genomic library containing the promoter region for the tracheobronchial mucin gene (TBM). The authenticity of the promoter was tested by nucleotide sequencing, primer extension analysis, electrophoretic mobility shift assay (EMSA) and reporter gene expression analysis. The canine TBM promoter is different from housekeeping gene promoters (as it is not rich in GC content and contains TATA- and CAAT-like sequences) and different from that of regulatory genes (because it contains many TATA- and CAAT-like sequences and multiple transcriptional initiation sites). Reporter gene analysis using canine TBM promoter-chloramphenicol acetyltransferase (CAT) fusion plasmids established the regions responsible for promoter activity and verified the positions of the major mucin transcriptional initiation sites. Reporter gene analysis also established that a region of the canine TBM promoter and first exon containing all of the transcriptional initiation sites is more active in mucin expressing cells (e.g. CT1 cells-immortalized canine tracheal epithelial cells, human CFT1 cells-immortalized tracheal epithelial cells from a CF subject, or HBE1 cells-immortalized tracheal epithelial cells from non-CF subject) than in mucin non-expressing cells (COS7, 3T3), suggesting cell specificity. The promoter region contained cAMP response element (CRE) sequences, and the TBM gene transcription was enhanced when cAMP analogs were added to transfected cells. EMSA indicated the presence of at least two DNA binding proteins in CT1 cells. This is the first report describing the characterization of a TBM gene promoter. The information obtained in the present studies will be valuable in understanding mucin gene regulation in normal and pathological conditions.
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