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The spatial distributions of both wall stress and wall strength are required to accurately evaluate the rupture potential for an individual abdominal aortic aneurysm (AAA). The purpose of this study was to develop a statistical model to non-invasively estimate the distribution of AAA wall strength. Seven parameters--namely age, gender, family history of AAA, smoking status, AAA size, local diameter, and local intraluminal thrombus (ILT) thickness--were either directly measured or recorded from the patients hospital chart. Wall strength values corresponding to these predictor variables were calculated from the tensile testing of surgically procured AAA wall specimens. Backwards-stepwise regression techniques were used to identify and eliminate insignificant predictors for wall strength. Linear mixed-effects modeling was used to derive a final statistical model for AAA wall strength, from which 95% confidence intervals on the model parameters were formed. The final statistical model for AAA wall strength consisted of the following variables: sex, family history, ILT thickness, and normalized transverse diameter. Demonstrative application of the model revealed a unique, complex wall strength distribution, with strength values ranging from 56 N/cm2 to 133 N/cm2. A four-parameter statistical model for the noninvasive estimation of patient-specific AAA wall strength distribution has been successfully developed. The currently developed model represents a first attempt towards the noninvasive assessment of AAA wall strength. Coupling this model with our stress analysis technique may provide a more accurate means to estimate patient-specific rupture potential of AAA.

This study compared arthroscopic biceps tenodesis with biceps repair for isolated type II superior labrum anterior and posterior (SLAP) lesions in patients older than 35 years. The authors identified isolated type II SLAP lesions that were surgically managed over a 5-year period. Minimum 2-year follow-up data were available for 22 patients who underwent biceps repair (repair group) and for 15 patients who underwent a primary biceps tenodesis (tenodesis group). Mean age at surgery was 45.2±5.5 years in the repair group and 52.0±8.0 years in the tenodesis group. In the repair group, functional outcome improved from baseline to final follow-up using the American Shoulder and Elbow Surgeons (ASES) (47.5 to 87.4, respectively; P <.0001) and University of California, Los Angeles (UCLA) scores (18.5 to 31.2, respectively; P <.0001). In the tenodesis group, similar findings were observed for the ASES (43.4 to 89.9, respectively; P <.0001) and UCLA scores (19.0 to 32.7, respectively; P <.0001). No difference was found in functional outcome between the groups. Full range of motion recovery was delayed by approximately 3 months in the repair group compared with the tenodesis group ( P =.0631). Two patients in the repair group required a secondary capsular release. Seventy-seven percent of patients in the repair group and 100% of patients in the tenodesis group were satisfied and returned to normal activity ( P =.0673). In the current study, individuals older than 35 years with an isolated type II SLAP lesion had a shorter postoperative recovery, a more predictable functional outcome, and a higher rate of satisfaction and return to activity with a biceps tenodesis compared with a biceps repair. Based on these observations, biceps tenodesis is preferable to biceps repair for isolated type II SLAP lesions in nonoverhead athletes older than 35 years.

To test the hypothesis that ruptured abdominal aortic aneurysms (AAA) are globally weaker than unruptured ones. Four ruptured and seven unruptured AAA specimens were harvested whole from fresh cadavers during autopsies performed over an 18-month period. Multiple regionally distributed longitudinally oriented rectangular strips were cut from each AAA specimen for a total of 77 specimen strips. Strips were subjected to uniaxial extension until failure. Sections from approximately the strongest and weakest specimen strips were studied histologically and histochemically. From the load-extension data, failure tension, failure stress and failure strain were calculated. Rupture site characteristics such as location, arc length of rupture and orientation of rupture were also documented. The failure tension, a measure of the tissue mechanical caliber was remarkably similar between ruptured and unruptured AAA (group mean±standard deviation of within-subject means: 11.2±2.3 versus 11.6±3.6N/cm; p=0.866 by mixed model ANOVA). In post-hoc analysis, there was little difference between the groups in other measures of tissue mechanical caliber as well such as failure stress (95±28 versus 98±23N/cm2; p=0.870), failure strain (0.39±0.09 versus 0.36±0.09; p=0.705), wall thickness (1.7±0.4 versus 1.5±0.4mm; p=0.470) , and % coverage of collagen within tissue cross section (49.6±12.9% versus 60.8±9.6%; p=0.133). In the four ruptured AAA, primary rupture sites were on the lateral quadrants (two on left; one on left-posterior; one on right). Remarkably, all rupture lines had a longitudinal orientation and ranged from 1 to 6cm in length. The findings are not consistent with the hypothesis that ruptured aortic aneurysms are globally weaker than unruptured ones. ► We studied whether ruptured abdominal aortic aneurysms are weaker than unruptured ones. ► Multiple specimens were obtained from each of 13 aneurysms harvested at necropsy. ► Specimen caliber was assessed by mechanical testing, histology and histochemistry. ► Ruptured aneurysms were not globally weaker than unruptured ones.

To assess whether survival differences exist between patients undergoing immediate open repair vs surveillance with selective repair for 4.0- to 5.4-cm abdominal aortic aneurysms (AAAs) and whether these differences vary by diameter, within sexes, or overall. The study cohort included 2226 patients randomized to immediate repair or surveillance for the UK Small Aneurysm Trial (September 1, 1991, through July 31, 1998; follow-up, 2.6-6.9 years) or the Aneurysm Detection and Management trial (August 1, 1992, through July 31, 2000; follow-up, 3.5-8.0 years). Survival differences were assessed with proportional hazard models, adjusted for a comprehensive array of clinical and nonclinical risk factors. Interaction between treatment and AAA size was added to the model to assess whether the effect of immediate open repair vs surveillance varied by AAA size. The adjusted analysis revealed no statistically significant survival difference between immediate open repair and surveillance patients (hazard ratio [HR], 0.99; 95% CI, 0.83-1.18; mean follow-up time, 1921 days for both study groups). This lack of treatment effect persisted when men (HR, 1.01; 95% CI, 0.84-1.21) and women (HR, 0.96; 95% CI, 0.49-1.86) were examined separately and did not vary by AAA size (P=.39 for the entire cohort and P=.24 for women). Immediate open repair offered no significant survival benefit, even in patients with the largest AAAs and highest risk of rupture. Because recent trials failed to find a survival benefit of immediate endovascular repair over surveillance for small asymptomatic AAAs, our findings suggest that the gray area of first-line management for these patients should be resolved in favor of surveillance.

Purpose To prospectively evaluate whether age of patient affects diagnostic accuracy of sonography and magnetic resonance imaging (MRI) in the diagnosis of medial meniscal tears. Methods We prospectively evaluated 74 consecutive patients (54 males and 20 females), in two different groups [group A (37 patients ≤ 30 years; mean age: 23.5 ± 5 years) and group B (37 patients > 30 years; mean age: 43.5 ± 9.35 years)] with clinical suspicion of medial meniscal tear. After inclusion, patients underwent ultrasonography and then MRI for signs of tearing. The ultrasonographic and MRI findings were compared with arthroscopic findings, which served as a gold standard for accurate detection of meniscal tearing. Results The sensitivity, specificity, positive and negative predictive values and accuracy of ultrasonography in detecting medial meniscal tears in group A were 100, 88.9, 96.5, 100, 97.3 % and in group B were 83.3, 71.4, 92.6, 50, 81.1 %, respectively. The sensitivity, specificity, positive and negative predictive values and accuracy of MRI in group A were 100, 88.9, 96.5, 100, 97.3 % and in group B were 96.7, 85.7, 96.7, 85.7, 94.6 %, respectively. Conclusions Given the fact that the sensitivity and specificity of the results of knee sonography matched that of MRI in patients who were 30 years old or less, we suggest ultrasonography as an effective initial investigation for tears of medial meniscus in this group of patients. Patients with negative ultrasonographic findings will need no further investigation. Level of evidence Diagnostic studies—investigating a diagnostic test, Level II.

Patients sometimes have left shoulder-tip pain caused by diaphragmatic irritation (Kehr's sign).4 Even a minor physical event, such as coughing, vomiting, or sneezing might cause rupture of a pathologically fragile, enlarged spleen,1,2 and treatment is quite different from that of blunt traumatic splenic rupture. Total splenectomy is the mainstay of treatment and also allows diagnosis of the underlying problem.1,2 A conservative, interventional, or spleen-preserving surgical approach should be attempted only in patients in whom the underlying cause is known to be benign.1 The effectiveness of post-splenectomy vaccinations and prophylactic antibiotic treatment is unclear after removal of a diseased spleen, and probably depends on the underlying cause.1,3

The integration of biomechanical and morphological analyses holds tremendous potential for assessing the rupture risk of abdominal aortic aneurysms (AAA). We employed a one-way fluid-structure interaction (FSI) model to distinguish between ruptured AAA (RAAA) and asymptomatic intact AAA (IAAA), focusing on morphological and computational fluid dynamics (CFD) indices. Patient groups with ruptured RAAA and asymptomatic IAAA were matched by diameter, age, and sex. AAA morphology was analyzed via CT segmentation, and biomechanical indices—including wall shear stress (WSS), peak wall stress (PWS), maximum deformation (MD), and other indices—were determined using FSI analysis. Statistical comparisons were performed using paired t-tests or Wilcoxon rank sum tests. Multivariate and LASSO regression analyses identified predictive factors, and a nomogram was developed. Model accuracy was assessed using the area under the curve (AUC). In our study with 66 RAAA and 66 asymptomatic IAAA patients, the tortuosity of the RAAAs was 1.4 times that of the asymptomatic IAAAs ( P  = 0.0005). The PWS, MD and peak wall rupture index (PWRI) of the RAAAs was 1.18, 1.32 and 1.27 times that of the asymptomatic IAAAs ( P  = 0.0158, 0.0036, 0.0071). The MD position demonstrated high consistency with RAAA rupture locations (94.12%). Four variables were selected for a nomogram, predicting AAA rupture with an AUC of 0.7604 (95% CI 0.6653–0.8556) and an internal validation AUC of 0.8051 (95% CI 0.6400–0.9703). In this study, we demonstrated that the location of MD is valuable for predicting the rupture location of AAA. We constructed a nomogram incorporating four key predictors—aortic neck length (ANL), intraluminal thrombus volume relative to AAA volume (VILT/VAAA), tortuosity, and MD—that enhances the prediction of AAA rupture risk, offering a more personalized assessment beyond traditional diameter-based methods.

BackgroundRecent investigation of human tissue and cells from positional tendons such as the rotator cuff has clarified the importance of inflammation in the development and progression of tendon disease. These mechanisms remain poorly understood in disease of energy-storing tendons such as the Achilles. Using tissue biopsies from patients, we investigated if inflammation is a feature of Achilles tendinopathy and rupture.MethodsWe studied Achilles tendon biopsies from symptomatic patients with either mid-portion tendinopathy or rupture for evidence of abnormal inflammatory signatures. Tendon-derived stromal cells from healthy hamstring and diseased Achilles were cultured to determine the effects of cytokine treatment on expression of inflammatory markers.ResultsTendinopathic and ruptured Achilles highly expressed CD14+ and CD68+ cells and showed a complex inflammation signature, involving NF-κB, interferon and STAT-6 activation pathways. Interferon markers IRF1 and IRF5 were highly expressed in tendinopathic samples. Achilles ruptures showed increased PTGS2 and interleukin-8 expression. Tendinopathic and ruptured Achilles tissues expressed stromal fibroblast activation markers podoplanin and CD106. Tendon cells isolated from diseased Achilles showed increased expression of pro-inflammatory and stromal fibroblast activation markers after cytokine stimulation compared with healthy hamstring tendon cells.ConclusionsTissue and cells derived from tendinopathic and ruptured Achilles tendons show evidence of chronic (non-resolving) inflammation. The energy-storing Achilles shares common cellular and molecular inflammatory mechanisms with functionally distinct rotator cuff positional tendons. Differences seen in the profile of ruptured Achilles are likely to be attributable to a superimposed phase of acute inflammation and neo-vascularisation. Strategies that target chronic inflammation are of potential therapeutic benefit for patients with Achilles tendon disease.

Infection of the genitourinary tract with Group B Streptococcus (GBS), an opportunistic gram positive pathogen, is associated with premature rupture of amniotic membrane and preterm birth. In this work, we demonstrate that GBS produces membrane vesicles (MVs) in a serotype independent manner. These MVs are loaded with virulence factors including extracellular matrix degrading proteases and pore forming toxins. Mice chorio-decidual membranes challenged with MVs ex vivo resulted in extensive collagen degradation leading to loss of stiffness and mechanical weakening. MVs when instilled vaginally are capable of anterograde transport in mouse reproductive tract. Intra-amniotic injections of GBS MVs in mice led to upregulation of pro-inflammatory cytokines and inflammation mimicking features of chorio-amnionitis; it also led to apoptosis in the chorio-decidual tissue. Instillation of MVs in the amniotic sac also resulted in intrauterine fetal death and preterm delivery. Our findings suggest that GBS MVs can independently orchestrate events at the feto-maternal interface causing chorio-amnionitis and membrane damage leading to preterm birth or fetal death.

High incidence of cardiac rupture in murine myocardial infarction (MI) model leads to a substantial loss before the study end-point. Selecting animal models with varying degrees of injury for different research purposes is crucial for cardiovascular research. Male C57 mice were subjected to ischemia/reperfusion (I/R) or permanent occlusion (MI) injury. The incidence of cardiac rupture, degree of myocardial injury, inflammatory responses, left ventricular (LV) remodeling and infarct myocardium healing were examined. Compared to MI mice, early reperfusion (1, 2 and 4h I/R) completely prevented cardiac rupture, while delayed reperfusion (12h and 24h I/R) significantly reduced incidence of cardiac rupture to 5.7% and 8.6%, respectively. In the acute phase, prolonged ischemia increased infarct size, myocyte apoptosis, and both systemic and regional inflammatory responses. These changes correspond to enhanced MMP-9 activity and a weakening of the tensile strength of the infarcted myocardium. Following ischemic insult, early reperfusion was associated with less extent of myocardial injury, inflammatory response and adverse cardiac remodeling, whereas, delayed reperfusion and MI groups exhibited severe myocardial damage and remodeling. Furthermore, both early and delayed reperfusion were associated with increased infiltration of type 2 macrophages and proliferation of endothelial cells during the early healing phase, thereby facilitating healing of the infarct myocardium. Delayed reperfusion resulted in a comparable and substantial degree of cardiac remodeling but with a lower risk of cardiac rupture in comparison with MI model. This feature makes it a feasible model for cardiac ischemia research.