The sacroiliac part of the iliolumbar ligament

The iliolumbar ligament has been described as the most important ligament for restraining movement at the lumbosacral junction. In addition, it may play an important role in restraining movement in the sacroiliac joints. To help understand its presumed restraining effect, the anatomy of the ligament and its orientation with respect to the sacroiliac joints were studied in 17 cadavers. Specific dissection showed the existence of several distinct parts of the iliolumbar ligament, among which is a sacroiliac part. This sacroiliac part originates on the sacrum and blends with the interosseous sacroiliac ligaments. Together with the ventral part of the iliolumbar ligament it inserts on the medial part of the iliac crest, separate from the interosseous sacroiliac ligaments. Its existence is verified by magnetic resonance imaging and by cryosectioning of the pelvis in the coronal and transverse plane. Fibre direction, length, width, thickness and orientation of the sacroiliac part of the iliolumbar ligament are described. It is mainly oriented in the coronal plane, perpendicular to the sacroiliac joint. The existence of this sacroiliac part of the iliolumbar ligament supports the assumption that the iliolumbar ligament has a direct restraining effect on movement in the sacroiliac joints

Anterior joint capsule of the normal hip and in children with transient synovitis: US study with anatomic and histologic correlation

PURPOSE: To study the anatomic components of the anterior joint capsule of the normal hip and in children with transient synovitis. MATERIALS AND METHODS: Six cadaveric specimens were imaged with ultrasonography (US) with special attention to the anterior joint capsule. Subsequently, two specimens were analyzed histologically. These anatomic findings were correlated with the US findings in 58 healthy children and 105 children with unilateral transient synovitis. RESULTS: The anterior joint capsule comprises an anterior and posterior layer, mainly composed of fibrous tissue, lined by only a minute synovial membrane. Both fibrous layers were identified separately at US in 98 of 116 (84%) hips of healthy subjects and in all hips with transient synovitis. Overall, the anterior layer was thicker than the posterior layer. In transient synovitis compared with normal hips, no significant thickening of both layers was present (P = .24 and .57 for the anterior and posterior layers, respectively). Normal variants include plicae, local thickening of the capsule, and pseudodiverticula. CONCLUSION: Increased thickness of the anterior joint capsule in transient synovitis is caused entirely by effusion. There is no US evidence for additional capsule swelling or synovial hypertrophy

MR-plastination-arthrography: A new technique used to study the distal tibiofibular syndesmosis

Purpose: The purpose of this study was to describe a new technique called MR plastination arthrography to study both intra- and extra-articular anatomy. Materials and methods: In six human cadaveric lower legs MR arthrography was performed in either a one-step or two-step procedure. In the former a mixture of diluted Gadolinium and dyed polymer was injected. In the latter the dyed polymer was injected after arthrography wih diluted Gadolinium. Three-millimeter slices of these legs, obtained in a plane identical to that of the MR images, were plastinated according to the E12 technique of von Hagens. The plastination slices were subsequently compared with the MR images. Results: The one-step procedure resulted in an inhomogeneous arthrogram. The two-step procedure resulted in a good correlation between the high-resolution MR images and plastination slices, as expressed by a good comparison of anatomic detail of the small syndesmotic recess. Conclusions: Images of the distal tibiofibular syndesmosis obtained with plastination arthrography correlated well with images acquired by MR arthrography when performed in a two-step procedure

Endoanal MRI of the anal sphincter complex: correlation with cross-sectional anatomy and histology

The purpose of this study was to correlate the in vivo endoanal MRI findings of the anal sphincter with the cross-sectional anatomy and histology. Fourteen patients with rectal tumours were examined with a rigid endoanal MR coil before undergoing abdominoperineal resection. In addition, 12 cadavers were used to obtain cross-sectional anatomical sections. The images were correlated with the histology and anatomy of the resected rectal specimens as well as with the cross-sectional anatomical sections of the 12 cadavers. The findings in 8 patients, 11 rectal preparations, and 10 cadavers, could be compared. In these cases, there was an excellent correlation between endoanal MRI and the cross-sectional cadaver anatomy and histology. With endoanal MRI, all muscle layers of the anal canal wall, comprising the internal anal sphincter, longitudinal muscle, the external anal sphincter and the puborectalis muscle wer

Sulindac targets nuclear β-catenin accumulation and Wnt signalling in adenomas of patients with familial adenomatous polyposis and in human colorectal cancer cell lines

Nonsteroidal anti-inflammatory drugs (NSAIDs) have chemopreventive potential against colorectal carcinomas (CRCs). Inhibition of cyclooxygenase (COX)-2 underlies part of this effect, although COX-2-independent mechanisms may also exist. Nonsteroidal anti-inflammatory drugs appear to inhibit the initial stages of the adenoma-carcinoma sequence, suggesting a link to the APC/beta-catenin/TCF pathway (Wnt-signalling pathway). Therefore, the effect of the NSAID sulindac on nuclear (nonphosphorylated) beta-catenin and beta-catenin/TCF-mediated transcription was investigated. Nuclear #946;-catenin expression was assessed in pretreatment colorectal adenomas and in adenomas after treatment with sulindac from five patients with familial adenomatous polyposis (FAP). Also, the effect of sulindac sulphide on beta-catenin/TCF-mediated transcription was studied. Adenomas of FAP patients collected after treatment with sulindac for up to 6 months showed less nuclear beta-catenin expression compared to pretreatment adenomas of the same patients. Sulindac sulphide abrogated beta-catenin/TCF-mediated transcription in the CRC cell lines DLD1 and SW480, and decreased the levels of nonphosphorylated beta-catenin. As a result, the protein levels of the positively regulated TCF targets Met and cyclin D1 were downregulated after sulindac treatment. This study provides in vivo and in vitro evidence that nuclear beta-catenin localisation and beta-catenin/TCF-regulated transcription of target genes can be inhibited by sulindac. The inhibition of Wnt-signalling provides an explanation for the COX-2-independent mechanism of chemoprevention by NSAID

Inflammatory Gene Haplotype-Interaction Networks Involved in Coronary Collateral Formation

Objectives: Formation of collateral circulation is an endogenous response to atherosclerosis, and is a natural escape mechanism by re-routing blood. Inflammatory responserelated genes underlie the formation of coronary collaterals. We explored the genetic basis of collateral formation in man postulating interaction networks between functional Single Nucleotide Polymorphisms (SNPs) in these inflammatory gene candidates. Methods: The contribution of 41 genes as well as the interactions among them was examined in a cohort of 226 coronary artery disease patients, genotyped for 54 candidate SNPs. Patients were classified to the extent of collateral circulation. Stepwise logistic regression analysis and a haplotype entropy procedure were applied to search for haplotype interactions among all 54 polymorphisms. Multiple testing was addressed by using the false discovery rate (FDR) method. Results: The population comprised 84 patients with and 142 without visible collaterals. Among the 41 genes, 16 pairs of SNPs were implicated in the development of collaterals with the FDR of 0.19. Nine SNPs were found to potentially have main effects on collateral formation. Two sets of coupling haplotypes that predispose to collateral formation were suggested. Conclusions: These findings suggest that collateral formation may arise from the interactions between several SNPs in inflammatory response related genes, which may represent targets in future studies of collateral formation. This may enhance developing strategies for risk stratification and therapeutic stimulation of arteriogenesis