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Purpose To define the bony attachments of the medial ligaments relative to anatomical and radiographic bony landmarks, providing information for medial collateral ligament (MCL) surgery. Method The femoral and tibial attachments of the superficial MCL (sMCL), deep MCL (dMCL) and posterior oblique ligament (POL), plus the medial epicondyle (ME) were defined by radiopaque staples in 22 knees. These were measured radiographically and optically; the precision was calculated and data normalised to the sizes of the condyles. Femoral locations were referenced to the ME and to Blumensaat’s line and the posterior cortex. Results The femoral sMCL attachment enveloped the ME, centred 1 mm proximal to it, at 37 ± 2 mm (normalised at 53 ± 2%) posterior to the most-anterior condyle border. The femoral dMCL attachment was 6 mm (8%) distal and 5 mm (7%) posterior to the ME. The femoral POL attachment was 4 mm (5%) proximal and 11 mm (15%) posterior to the ME. The tibial sMCL attachment spread from 42 to 71 mm (81–137% of A-P plateau width) below the tibial plateau. The dMCL fanned out anterodistally to a wide tibial attachment 8 mm below the plateau and between 17 and 39 mm (33–76%) A-P. The POL attached 5 mm below the plateau, posterior to the dMCL. The 95% CI intra-observer was ± 0.6 mm, inter-observer ± 1.3 mm for digitisation. The inter-observer ICC for radiographs was 0.922. Conclusion The bone attachments of the medial knee ligaments are located in relation to knee dimensions and osseous landmarks. These data facilitate repairs and reconstructions that can restore physiological laxity and stability patterns across the arc of knee flexion.

We show that collateral plays an important role in the design of debt contracts, the provision of credit, and the incentives of lenders to monitor borrowers. Using a unique data set from a large bank containing timely assessments of collateral values, we find that the bank responded to a legal reform that exogenously reduced collateral values by increasing interest rates, tightening credit limits, and reducing the intensity of its monitoring of borrowers and collateral, spurring borrower delinquency on outstanding claims. We thus explain why banks are senior lenders and quantify the value of claimant priority.

Purpose In anterior cruciate ligament (ACL) injuries, concomitant damage to peripheral soft tissues is associated with increased rotatory instability of the knee. The purpose of this study was to investigate the incidence and patterns of medial collateral ligament complex injuries in patients with clinically ‘isolated’ ACL ruptures. Methods Patients who underwent ACL reconstruction for complete ‘presumed isolated’ ACL rupture between 2015 and 2019 were retrospectively included in this study. Patient’s characteristics and intraoperative findings were retrieved from clinical and surgical documentation. Preoperative MRIs were evaluated and the grade and location of injuries to the superficial MCL (sMCL), dMCL and the posterior oblique ligament (POL) recorded. All patients were clinically assessed under anaesthesia with standard ligament laxity tests. Results Hundred patients with a mean age of 22.3 ± 4.9 years were included. The incidence of concomitant MCL complex injuries was 67%. sMCL injuries occurred in 62%, dMCL in 31% and POL in 11% with various injury patterns. A dMCL injury was significantly associated with MRI grade II sMCL injuries, medial meniscus ‘ramp’ lesions seen at surgery and bone oedema at the medial femoral condyle (MFC) adjacent to the dMCL attachment site ( p  < 0.01). Logistic regression analysis identified younger age (OR 1.2, p  < 0.05), simultaneous sMCL injury (OR 6.75, p  < 0.01) and the presence of bone oedema at the MFC adjacent to the dMCL attachment site (OR 5.54, p  < 0.01) as predictive factors for a dMCL injury. Conclusion The incidence of combined ACL and medial ligament complex injuries is high. Lesions of the dMCL were associated with ramp lesions, MFC bone oedema close to the dMCL attachment, and sMCL injury. Missed AMRI is a risk factor for ACL graft failure from overload and, hence, oedema in the MCL (especially dMCL) demands careful assessment for AMRI, even in the knee lacking excess valgus laxity. This study provides information about specific MCL injury patterns including the dMCL in ACL ruptures and will allow surgeons to initiate individualised treatment. Level of evidence III.

Purpose To define the length-change patterns of the superficial medial collateral ligament (sMCL), deep MCL (dMCL), and posterior oblique ligament (POL) across knee flexion and with applied anterior and rotational loads, and to relate these findings to their functions in knee stability and to surgical repair or reconstruction. Methods Ten cadaveric knees were mounted in a kinematics rig with loaded quadriceps, ITB, and hamstrings. Length changes of the anterior and posterior fibres of the sMCL, dMCL, and POL were recorded from 0° to 100° flexion by use of a linear displacement transducer and normalised to lengths at 0° flexion. Measurements were repeated with no external load, 90 N anterior draw force, and 5 Nm internal and 5 Nm external rotation torque applied. Results The anterior sMCL lengthened with flexion ( p  < 0.01) and further lengthened by external rotation ( p  < 0.001). The posterior sMCL slackened with flexion ( p  < 0.001), but was lengthened by internal rotation ( p  < 0.05). External rotation lengthened the anterior dMCL fibres by 10% throughout flexion ( p  < 0.001). sMCL release allowed the dMCL to become taut with valgus rotation ( p  < 0.001). The anterior and posterior POL fibres slackened with flexion ( p  < 0.001), but were elongated by internal rotation ( p  < 0.001). Conclusion The structures of the medial ligament complex react differently to knee flexion and applied loads. Structures attaching posterior to the medial epicondyle are taut in extension, whereas the anterior sMCL, attaching anterior to the epicondyle, is tensioned during flexion. The anterior dMCL is elongated by external rotation. These data offer the basis for MCL repair and reconstruction techniques regarding graft positioning and tensioning.

Cardiovascular disease remains the leading global cause of death, and the number of patients with coronary artery disease (CAD) and exhausted therapeutic options (i.e., percutaneous coronary intervention (PCI), coronary artery bypass grafting (CABG) and medical treatment) is on the rise. Therefore, the evaluation of new therapeutic approaches to offer an alternative treatment strategy for these patients is necessary. A promising research field is the promotion of the coronary collateral circulation, an arterio-arterial network able to prevent or reduce myocardial ischemia in CAD. This review summarizes the basic principles of the human coronary collateral circulation, its extracardiac anastomoses as well as the different therapeutic approaches, especially that of stimulating the extracardiac collateral circulation via permanent occlusion of the internal mammary arteries.

Purpose The purpose of the present study was to determine how the medial structures and ACL contribute to restraining anteromedial instability of the knee. Methods Twenty-eight paired, fresh-frozen human cadaveric knees were tested in a six-degree of freedom robotic setup. After sequentially cutting the dMCL, sMCL, POL and ACL in four different cutting orders, the following simulated clinical laxity tests were applied at 0°, 30°, 60° and 90° of knee flexion: 4 Nm external tibial rotation (ER), 4 Nm internal tibial rotation (IR), 8 Nm valgus rotation (VR) and anteromedial rotation (AMR)—combined 89 N anterior tibial translation and 4 Nm ER. Knee kinematics were recorded in the intact state and after each cut using an optical tracking system. Differences in medial compartment translation (AMT) and tibial rotation (AMR, ER, IR, VR) from the intact state were then analyzed. Results The sMCL was the most important restraint to AMR, ER and VR at all flexion angles. Release of the proximal tibial attachment of the sMCL caused no significant increase in laxity if the distal sMCL attachment remained intact. The dMCL was a minor restraint to AMT and ER. The POL controlled IR and was a minor restraint to AMT and ER near extension. The ACL contributed with the sMCL in restraining AMT and was a secondary restraint to ER and VR in the MCL deficient knee. Conclusion The sMCL appears to be the most important restraint to anteromedial instability; the dMCL and POL play more minor roles. Based on the present data a new classification of anteromedial instability is proposed, which may support clinical examination and treatment decision. In higher grades of anteromedial instability an injury to the sMCL should be suspected and addressed if treated surgically.

We show that collateral constraints restrict firm entry and postentry growth, using French administrative data and cross-sectional variation in local house-price appreciation as shocks to collateral values. We control for local demand shocks by comparing treated homeowners to controls in the same region that do not experience collateral shocks: renters and homeowners with an outstanding mortgage, who (in France) cannot take out a second mortgage. In both comparisons, an increase in collateral value leads to a higher probability of becoming an entrepreneur. Conditional on entry, treated entrepreneurs use more debt, start larger firms, and remain larger in the long run.

We build a macrofinance model of shadow banking—the transformation of risky assets into securities that are money-like in quiet times but become illiquid when uncertainty spikes. Shadow banking economizes on scarce collateral, expanding liquidity provision, boosting asset prices and growth, but also building up fragility. A rise in uncertainty raises shadow banking spreads, forcing financial institutions to switch to collateral-intensive funding. Shadow banking collapses, liquidity provision shrinks, liquidity premia and discount rates rise, asset prices and investment fall. The model generates slow recoveries, collateral runs, and flight-to-quality effects, and it sheds light on Large-Scale Asset Purchases, Operation Twist, and other interventions.

Understanding the anatomy of the ankle ligaments is important for correct diagnosis and treatment. Ankle ligament injury is the most frequent cause of acute ankle pain. Chronic ankle pain often finds its cause in laxity of one of the ankle ligaments. In this pictorial essay, the ligaments around the ankle are grouped, depending on their anatomic orientation, and each of the ankle ligaments is discussed in detail.

Collaterals are unique blood vessels present in the microcirculation of most tissues that, by cross-connecting a small fraction of the outer branches of adjacent arterial trees, provide alternate routes of perfusion. However, collaterals are especially susceptible to rarefaction caused by aging, other vascular risk factors, and mouse models of Alzheimer’s disease—a vulnerability attributed to the disturbed hemodynamic environment in the watershed regions where they reside. We examined the hypothesis that endothelial and smooth muscle cells (ECs and SMCs, respectively) of collaterals have specializations, distinct from those of similarly-sized nearby distal-most arterioles (DMAs) that maintain collateral integrity despite their continuous exposure to low and oscillatory/disturbed shear stress, high wall stress, and low blood oxygen. Examination of mouse brain revealed the following: Unlike the pro-inflammatory cobble-stoned morphology of ECs exposed to low/oscillatory shear stress elsewhere in the vasculature, collateral ECs are aligned with the vessel axis. Primary cilia, which sense shear stress, are present, unexpectedly, on ECs of collaterals and DMAs but are less abundant on collaterals. Unlike DMAs, collaterals are continuously invested with SMCs, have increased expression of Pycard, Ki67, Pdgfb, Angpt2, Dll4, Ephrinb2, and eNOS, and maintain expression of Klf2/4. Collaterals lack tortuosity when first formed during development, but tortuosity becomes evident within days after birth, progresses through middle age, and then declines—results consistent with the concept that collateral wall cells have a higher turnover rate than DMAs that favors proliferative senescence and collateral rarefaction. In conclusion, endothelial and SMCs of collaterals have morphologic and functional differences from those of nearby similarly sized arterioles. Future studies are required to determine if they represent specializations that counterbalance the disturbed hemodynamic, pro-inflammatory, and pro-proliferative environment in which collaterals reside and thus mitigate their risk factor-induced rarefaction.